Clusterin as a potential marker of brain ischemia-reperfusion injury in patients undergoing carotid endarterectomy.

Introduction: Carotid endarterectomy (CEA) is a surgical procedure used in the prevention of ischemic stroke. However, this procedure can cause complications of ischemia-reperfusion injury to the brain. Clusterin (CLU) is a cytoprotective chaperone protein that is released from neurons in response to various neurological injuries. The objective of the study was to report the changes in serum CLU concentrations of patients undergoing CEA. Materials and methods: The study involved 25 patients with severe internal carotid artery stenosis. Serum samples were taken from patients at three different times: within 24 hours preoperatively to CEA, 12 hours postoperatively, and 48 hours postoperatively. Serum CLU concentrations were measured using a commercially available enzyme-linked immunosorbent assay. Results: When compared to concentrations preoperatively, the serum CLU concentration initially decreased during the 12 hours following CEA. However, 48 hours following the procedure there was an increase in the CLU concentration. After statistical analysis, differences were detected in serum CLU concentration between all three recorded measurements (P < 0.05). Conclusion: Data from our study indicate that serum CLU concentrations are affected after CEA. We hypothesize that serum CLU concentrations may depend on brain ischemia-reperfusion injury following this surgical procedure.

Serum Neuron-Specific Enolase as a Marker of Brain Ischemia-Reperfusion Injury in Patients Undergoing Carotid Endarterectomy

In patients with atherosclerotic stenosis of the extracranial segment of internal carotid artery, surgical intervention is an effective method to prevent cerebral ischemic stroke. However, this surgical procedure may cause vascular brain damage. The aim of the study was to investigate consequential brain ischemia-reperfusion injury by measuring the cerebral specific marker, neuron-specific (NSE), in serum of patients having undergone internal carotid endarterectomy (CEA). The study involved 25 patients that underwent CEA due to internal carotid artery stenosis. Blood samples were obtained from each patient on three occasions: within 24 h prior to surgery, 12 h after surgery, and 48 h after surgery. Serum NSE levels were measured by a commercially available enzyme-linked immunosorbent assay. The study showed that serum NSE level was statistically significantly increased 48 h after CEA as compared with the level 12 h after surgery and the level before surgery (p<0.05). Difference in serum NSE between the level before surgery and 12 h after CEA was not statistically significant (p>0.05). Data from our study showed CEA to affect serum NSE in patients with significant internal carotid artery stenosis. Thus, serum NSE may be used as a biochemical marker of brain ischemia-reperfusion injury following CEA.

Serum soluble OX40 in patients with amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease. Data from the literature show that systemic immune activation plays a role in ALS. OX40 (CD134) is member of the tumor necrosis factor receptor family and is expressed selectively on activated T lymphocytes. The aim of the study was to measure serum soluble OX40 (sOX40) levels in patients with ALS. The study included 25 ALS patients and 15 control subjects. Serum sOX40 levels were determined by the enzyme-linked immunosorbent method. Study showed that sOX40 levels were significantly decreased in serum of ALS patients compared with controls (P=0.05). There was no significant correlation between serum sOX40 levels and clinical parameters ofALS such as severity of the ALS patient clinical state and duration of the disease (P>0.05). In conclusion, decrease in serum sOX40 levels in patients with ALS suggests that this cytokine may be implicated in the pathomechanisms of this disease.

Serum caspase-9 levels are increased in patients with amyotrophic lateral sclerosis.

It is known that apoptosis may play a role in the pathophysiology of amyotrophic lateral sclerosis (ALS). Moreover, caspase-9 is implicated in the apoptosis pathway. The aim of the study was to investigate caspase-9 levels in serum of patients with ALS. The study involved 30 patients with ALS and 30 patients from the control group. The serum caspase-9 levels were measured using the enzyme-linked immunosorbent method. The study showed that caspase-9 levels are significantly increased in serum of the patients with ALS comparing to the control group (p < 0.05). There was a significant correlation of serum caspase-9 levels with severity of clinical state of ALS patients and duration of the disease (p < 0.05). The results indicate that caspase-9 may be implicated in pathomechanism of neurodegeneration in ALS.

Granzymes A and B levels in serum of patients with amyotrophic lateral sclerosis.

OBJECTIVES: There are evidences that immuno-inflammatory mechanisms and apoptosis may play a role in the pathophysiology of amyotrophic lateral sclerosis (ALS). It is known that Granzyme A (GzmA) and granzyme B (GzmB) are implicated in these mechanisms. The aim of the study was to investigate serum GzmA and GzmB levels in patients with ALS. DESIGN AND METHODS: The study included 30 patients with ALS and 30 patients from the control group. Serum GzmA and GzmB levels were measured using the enzyme-linked immunosorbent method. RESULTS: The study showed that GzmA and GzmB levels are significantly increased in serum of patients with ALS when compared to the control group (p<0.05). There was a significant correlation of serum GzmB levels with severity of clinical state of ALS patients (p<0.05). CONCLUSION: The results indicate that GzmA and GzmB are implicated in mechanisms of neurodegeneration in ALS.

Cerebrospinal fluid angiogenin level in patients with amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease. It is suggested that angiogenin (ANG) may play a role in the pathomechanism of this disease. The aim of the study was to measure cerebrospinal fluid (CSF) ANG levels in patients with ALS. Twenty ALS patients and 15 control subjects were included in the study. CSF ANG levels were measured by ELISA. Study results showed that CSF ANG level did not differ between ALS patients and control group (p > 0.05). There was no significant correlation between CSF ANG level and clinical state of ALS patients either (p > 0.05). The present study conducted on CSF of patients with ALS did not confirm previous observation on the possible role of ANG in neurodegeneration in this disease.

[Multiple ischemic foci of the brain in female patient with cardiac myxoma and numerous vascular anomalies]. / Mnogie ogniska niedokrwienne mózgu u pacjentki ze sluzakiem serca i licznymi anomaliami naczyniowymi.

The ischemic stroke is the most frequent neurological pathology. It's etiology is quite complex. Around 20% of the ischemic stroke cases are caused by arteriosclerosis, 25% by lacunar stroke, remaining 30% are strokes with unclear etiology, around 20%--emboli, and 5% include other causes. The ischemic stroke, especially in younger patients suggests that a detailed and multidimensional diagnostic should be carried out. Presented the case of a female patient with multiple ischemic foci of the brain, whom cardiac myxoma and numerous vascular anomalies were detected. Ischemic foci of the brain might be caused by myxoma, but one cannot excluded other mechanism of their occurrence.

Does VEGF represent a potential treatment for amyotrophic lateral sclerosis?

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease. The pathogenesis of ALS is unclear and there is no effective treatment. Vascular endothelial growth factor (VEGF) is a cytokine that has a protective function via angiogenic, neurotrophic, gliotrophic and anti-apoptotic activity. Data indicate that VEGF can inhibit neurodegeneration in ALS and may have therapeutic potential in this disease. The use of gene therapy to deliver VEGF into the central nervous system is being evaluated.

APRIL is increased in serum of patients with brain glioblastoma multiforme.

A PRoliferation-Inducing Ligand (APRIL) is a cytokine with the ability to induce tumorigenesis. The aim of the study was to measure serum APRIL levels in patients with brain glioblastoma multiforme. Twenty five patients with brain tumor and a control group of 25 subjects took part in the study. APRIL was measured by the enzyme-linked immunosorbent method. The study showed increased APRIL levels in the serum of patients with brain glioblastoma multiforme compared to the control group (p < 0.05). However, there was no significant difference in the level of this cytokine between groups of patients divided according to their clinical state and tumor size (p > 0.05). Inflammation parameters such as C-reactive protein (CRP) and polymorphonuclear leucocytes (PMN) were also increased in patients with brain tumor compared to controls (p < 0.05). There was a significant correlation between APRIL and CRP and PMN (p < 0.05). Results from the study suggest that APRIL may play a role in the pathogenesis of brain glioblastoma multiforme. It is possible that anti-APRIL therapy might be useful in this disease. However, this cytokine cannot be regarded as a marker of tumor size or of severity of the clinical condition of patients.

Cerebrospinal fluid vascular endothelial growth factor in patients with amyotrophic lateral sclerosis.

Oxidative stress and glutamate-mediated toxicity may play an important role in the etiopathogenesis of amyotrophic lateral sclerosis (ALS). The vascular endothelial growth factor (VEGF) is a neuroprotective cytokine activated by hypoxia. The aim of this study was to measure VEGF levels in the cerebrospinal fluid (CSF) of ALS patients. The study concerned 30 ALS patients and 30 control subjects. The VEGF was measured by the enzyme-linked immunosorbent assay. The results have shown that CSF VEGF levels are significantly increased in patients with long duration of ALS and in patients with limb-onset of the disease compared with controls (P < 0.05). Moreover, the type of ALS patients' subgroup significantly influences CSF VEGF levels (P = 0.05). The CSF VEGF levels were significantly increased in patients with limb-onset compared to patients with bulbar-onset of ALS, and in patients with long duration of ALS compared to patients with its short duration (P < 0.05). There was a significant correlation between CSF VEGF levels and duration of ALS (P < 0.05). It seems that a significant increase in CSF VEGF levels in patients with limb-onset of ALS and in patients with long duration of the disease may have a protective role against glutamate-mediated toxicity and oxidative damage of motor neurons. However, the conclusions are limited due to relatively small subgroups of ALS patients and by lack of a control group consisting of healthy persons. Further investigations could help to confirm the results from this preliminary report.

Increased serum CNTF level in patients with amyotrophic lateral sclerosis.

The role of ciliary neurotrophic factor (CNTF) in the etiopathogenesis of amyotrophic lateral sclerosis (ALS) is still not clear. The aim of this study was to measure serum CNTF level in patients with ALS. The study involved 36 ALS patients and 43 control group subjects. CNTF was measured by the enzyme-linked immunosorbent assay. Results showed that the serum CNTF level in whole group of ALS patients was significantly higher from those in the total control group subjects. CNTF level was not dependent on the clinical state of the ALS patients, type of ALS onset, or duration of the disease. Results indicate that CNTF may be a reactive component resulting from the disease, but it cannot be a marker of ALS activity. It is possible that the increase in serum CNTF level is the result of the muscle denervation seen in this disease.

Serum bilirubin concentration in patients with amyotrophic lateral sclerosis.

Oxidative stress plays probably an important role in the etiopathogenesis of amyotrophic lateral sclerosis (ALS). It is known that bilirubin (BR) is an endogenous antioxidant. The aim of this study was to evaluate serum BR concentration in ALS patients. BR was determined by automated analyzer in the serum from 30 ALS and 26 healthy control group people. The study showed that serum BR concentration is significantly decreased in ALS patients with a long duration of ALS compared with patients with a short duration (P<0.05), and it is also significantly decreased in ALS patients with a moderate clinical state compared with control group patients (P<0.05). There was no significant difference in BR concentration between the groups of patients classified according to their age and sex, the clinical state, and the type of ALS onset (P>0.05). Results suggest a possibility of endogenous antioxidant system dysfunction in later phase of ALS. A decrease in BR concentration might diminish its protective effect against oxidative injury and could accelerate motor neuron degeneration.

Thyroid function in patients with amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting motor neurons. Etiopathogenesis of the disease is not known. It is supposed that immunological disturbances play a role, which is among others confirmed by coexistence of ALS with autoimmunological disorders, including thyroid diseases. The aim of the study was to investigate the thyroid function in ALS through the measurement of triiodothyronine (T3), thyroxine (T4), and thyroid stimulating hormone (TSH) in the serum of ALS patients. The hormones level was measured by radioimmunoassay method. The study showed that the hormones level in ALS patients was not different from controls, and the clinical parameters of the disease did not influence the measured hormones level.

Increased serum levels of endogenous protectant secretory leukocyte protease inhibitor in acute ischemic stroke patients.

BACKGROUND: Activated leukocytes and their mediators may participate in ischemic brain injury. Secretory leukocyte protease inhibitor (SLPI) plays an important role in regulating the activity of the proteases, and may limit tissue damage. The aim of this study was to evaluate the changes in SLPI level in ischemic stroke patients. METHODS: The study comprised 20 patients with ischemic stroke and 20 controls. SLPI levels were measured in serum using enzyme-linked immunosorbent assay on the 1st, 5th and 12th day after stroke onset. RESULTS: SLPI was increased in the whole group of ischemic stroke patients compared with controls. It was also significantly increased on the 1st, 5th and 12th day after stroke in patients with larger brain tissue damage involving one or more lobe of the brain and in patients with more severe clinical status compared to controls (p < 0.05). A significant correlation between SLPI and the extent of brain tissue damage was observed on the 12th day after ischemic stroke onset (p < 0.05). CONCLUSIONS: Our results suggest that SLPI takes part in the anti-inflammatory reaction after ischemic stroke. Endogenous SLPI may have a neuroprotective effect, and could be a prototype therapeutic approach for ischemic stroke.

Transforming growth factor-Beta 1 (tgf-Beta 1) in patients with amyotrophic lateral sclerosis.

Previous investigations have shown that the transforming growth factor-beta 1 (TGF-beta 1) may protect neurons against excitotoxic and oxidative damage and may inhibit apoptosis. The aim of this study was to investigate the role of TGF-beta 1 in patients with amyotrophic lateral sclerosis (ALS). The study involved 24 ALS patients and 15 control group people. The ALS patients were divided into groups according to their clinical status, and duration of ALS. The TGF-beta 1 in the serum and cerebrospinal fluid (CSF) was measured by the enzyme-linked immunosorbent assay (ELISA). Results showed that TGF-beta 1 concentrations in the serum, and CSF in the whole group of ALS patients did not differ from those of the controls, but the serum TGF-beta 1 concentration was significantly higher in ALS patients with a terminal clinical status than in controls. The TGF-beta 1 concentration was significantly higher in the CSF of the patients, with a long duration of ALS, than in the patients with a short duration of ALS, and there was a significant positive correlation between the CSF TGF-beta 1 and the duration of ALS. TGF-beta 1 may play a role in neurodegeneration of ALS, and may be an indicator of the duration of the disease.