OBJECTIVES: The purpose is to investigate effect of septoplasty and widened nasal patency on voice quality. METHODS: Fifty patients who undergone septoplasty were included in the study. Thirty-three people who had similar age and distribution were enrolled as control group. Before and 1 and 3 months after surgery, anterior rhinomanometry, voice analysis by Multi-Dimensional Voice Program, and spectrographic analysis were performed to patients. The recordings of /a/ vowel were used to evaluate average fundamental frequency (F0), jitter percent, and shimmer percent. In spectrographic analyses, F3–F4 values for the vowels /i, e, a, o, and u/, nasal formant frequencies of the consonants /m/ and /n/ in the word /mini/, and 4 formant frequencies (F1, F2, F3, and F4) for nasalized /i/ vowel following a nasal consonant /n/ in the word /mini/ were compared. The differences in nasal resonance were evaluated. All patients were asked whether change in their voices after the surgery. Preoperative and postoperative voice parameters and anterior rhinomanometry results were compared separately with the control group as well as in the patient group itself. RESULTS: Preoperative total nasal resistance (TNR) values of patients were higher than the control group (P=0.001). TNR values of patients measured one day before surgery and after surgery in the 1st and 3rd months were different and these differences were significant statistically (P=0.001). There was no significant difference between the voice analysis parameters in preoperative, postoperative 1st, and 3rd months. As a result of their subjective reviews, 12 patients (36%) noted their voices were better than before surgery and 20 patients (61%) noted no change before and after surgery. CONCLUSION: Providing widened nasal cavity has no effect on voice quality.
Humans ; Nasal Cavity ; Nasal Septum ; Rhinomanometry ; Voice Quality* ; Voice*

Pseudotumor cerebri is a condition of increased intracranial pressure in the absence of clinical, laboratory or radiological pathology. Spinal intradural hematoma formation after lumboperitoneal shunt (LPS) implantation is very rare, but it can cause sudden and serious deterioration. In this report, we present a patient who developed an intradural hematoma following LPS operation. A 27-year-old male patient suffering from headaches and progressive vision loss was diagnosed with pseudotumor cerebri. He underwent LPS operation in January 2009. Four hours after the operation, he developed urinary and fecal incontinence with paraparesis (1/5). Lumbar magnetic resonance imaging identified an intradural hematoma at the level of L2-L3, and he was reoperated. The intradural hematoma was removed. Physical therapy was started because of paraparesis. Two months later, the patient's muscle strength had increased to 3/5. Surgeons must remember that, LPS implantation can cause a spinal intradural hematoma in a small percentage of patients, with catastrophic results.
Adult ; Fecal Incontinence ; Headache ; Hematoma* ; Humans ; Intracranial Pressure ; Magnetic Resonance Imaging ; Male ; Muscle Strength ; Paraparesis* ; Pathology ; Polyradiculopathy ; Pseudotumor Cerebri

Pseudotumor cerebri is a condition of increased intracranial pressure in the absence of clinical, laboratory or radiological pathology. Spinal intradural hematoma formation after lumboperitoneal shunt (LPS) implantation is very rare, but it can cause sudden and serious deterioration. In this report, we present a patient who developed an intradural hematoma following LPS operation. A 27-year-old male patient suffering from headaches and progressive vision loss was diagnosed with pseudotumor cerebri. He underwent LPS operation in January 2009. Four hours after the operation, he developed urinary and fecal incontinence with paraparesis (1/5). Lumbar magnetic resonance imaging identified an intradural hematoma at the level of L2-L3, and he was reoperated. The intradural hematoma was removed. Physical therapy was started because of paraparesis. Two months later, the patient's muscle strength had increased to 3/5. Surgeons must remember that, LPS implantation can cause a spinal intradural hematoma in a small percentage of patients, with catastrophic results.
Adult ; Fecal Incontinence ; Headache ; Hematoma* ; Humans ; Intracranial Pressure ; Magnetic Resonance Imaging ; Male ; Muscle Strength ; Paraparesis* ; Pathology ; Polyradiculopathy ; Pseudotumor Cerebri

Objective: NOD-like receptor protein 1 (NLRP1) inflammasome complex has been recently associated with chronic unpredictablemild stress (CUMS) model of depression. Our aim was to investigate whether ketamine-induced antidepressant effect is associated withsuppression of NLRP1. Methods: Wistar albino rats were divided into control, CUMS, CUMS+acute ketamine (a single 10 mg/kg dose) and CUMS+chronicketamine (daily 10 mg/kg injections for 3 weeks) groups (n=10 for each group). Sucrose preference test and forced swimming test wereperformed to assess anhedonia and immobility time respectively for the severety of depression symptoms. Brain tissues were dissectedand prefrontal cortex and hippocampus regions were used for real-time polymerase chain reaction (PCR) and immunohistochemicalanalysis. Results: CUMS procedure significantly induced depressive-like symptoms whereas both acute and chronic ketamine treatment amelioratedthem. mRNA expression levels of NLRP1, caspase 1, apoptosis-associated speck-like protein containing a CARD (ASC), NF-κB,endothelial nitric oxide synthase, IL-1β, IL-6, toll-like receptor 4 (TLR-4) and purinergic 2×7 receptor (P2X7R) and numbers of Iba-1+and GFAP+glial cells were reduced by acute and/or chronic ketamine treatment. Conclusion In the present study for the first time upstream and downstream elements of the NLRP1 inflammasome complex are shownto be suppressed by ketamine thus reinforcing the involvement of NLRP1 in the physiopathology of depression.Psychiatry Investig 2020;17(4):283-291

Objective: : Dexpanthenol (DXP), which has known neuroprotective effects, has been shown to be beneficial in various experimental models and ischaemic diseases. The aim of this study was to investigate the possible neuroprotective effects of DXP in a traumatic brain injury (TBI) model. Methods: : Thirty-six Wistar-Albino female rats, approximately 6 months old, weighing 220–285 g were used. All rats were subjected to closed head trauma by dropping a weight of 350 g on the parietal region from a height of 50 cm at an angle of 180 degrees in the prepared head trauma model setup. The rats were divided into four groups as control (group 1), trauma (group 2), trauma + DXP (group 3), and DXP (group 4). In group 3, DXP was administered intraperitoneally at a dose of 500 mg/kg for six times at 30 minutes, 6, 12, 24, 36, and 48 hours. In group 4, DXP was administered intraperitoneally simultaneously with group 3 without causing head trauma. Blood samples were taken from all rats 72 hours later for biochemical examination. After blood samples were taken, rats were decapitated under general anaesthesia. Cerebral tissue samples were taken from decapitated rats for immunohistochemical and histopathological examination. Results: : Cytokine markers were found to be increased in posttraumatic brain tissue. Malondialdehyde and glutathione reductase levels were lower in group 3 compared to group 2. In addition, superoxide dismutase, glutathione peroxidase and catalase levels were significantly higher in group 3 compared to group 2. In histological evaluation, congestion in the piamater layer, cell infiltration, vascular congestion, hemorrhage and neuronal degeneration were significantly decreased in group 3 compared to group 2. DXP seems to be beneficial in neurological recovery in terms of histological and oxidative changes after head trauma in rats. Conclusion : DXP should be further evaluated for its possible therapeutic effect in TBI.

Objective: : Dexpanthenol (DXP), which has known neuroprotective effects, has been shown to be beneficial in various experimental models and ischaemic diseases. The aim of this study was to investigate the possible neuroprotective effects of DXP in a traumatic brain injury (TBI) model. Methods: : Thirty-six Wistar-Albino female rats, approximately 6 months old, weighing 220–285 g were used. All rats were subjected to closed head trauma by dropping a weight of 350 g on the parietal region from a height of 50 cm at an angle of 180 degrees in the prepared head trauma model setup. The rats were divided into four groups as control (group 1), trauma (group 2), trauma + DXP (group 3), and DXP (group 4). In group 3, DXP was administered intraperitoneally at a dose of 500 mg/kg for six times at 30 minutes, 6, 12, 24, 36, and 48 hours. In group 4, DXP was administered intraperitoneally simultaneously with group 3 without causing head trauma. Blood samples were taken from all rats 72 hours later for biochemical examination. After blood samples were taken, rats were decapitated under general anaesthesia. Cerebral tissue samples were taken from decapitated rats for immunohistochemical and histopathological examination. Results: : Cytokine markers were found to be increased in posttraumatic brain tissue. Malondialdehyde and glutathione reductase levels were lower in group 3 compared to group 2. In addition, superoxide dismutase, glutathione peroxidase and catalase levels were significantly higher in group 3 compared to group 2. In histological evaluation, congestion in the piamater layer, cell infiltration, vascular congestion, hemorrhage and neuronal degeneration were significantly decreased in group 3 compared to group 2. DXP seems to be beneficial in neurological recovery in terms of histological and oxidative changes after head trauma in rats. Conclusion : DXP should be further evaluated for its possible therapeutic effect in TBI.

Objective: : Dexpanthenol (DXP), which has known neuroprotective effects, has been shown to be beneficial in various experimental models and ischaemic diseases. The aim of this study was to investigate the possible neuroprotective effects of DXP in a traumatic brain injury (TBI) model. Methods: : Thirty-six Wistar-Albino female rats, approximately 6 months old, weighing 220–285 g were used. All rats were subjected to closed head trauma by dropping a weight of 350 g on the parietal region from a height of 50 cm at an angle of 180 degrees in the prepared head trauma model setup. The rats were divided into four groups as control (group 1), trauma (group 2), trauma + DXP (group 3), and DXP (group 4). In group 3, DXP was administered intraperitoneally at a dose of 500 mg/kg for six times at 30 minutes, 6, 12, 24, 36, and 48 hours. In group 4, DXP was administered intraperitoneally simultaneously with group 3 without causing head trauma. Blood samples were taken from all rats 72 hours later for biochemical examination. After blood samples were taken, rats were decapitated under general anaesthesia. Cerebral tissue samples were taken from decapitated rats for immunohistochemical and histopathological examination. Results: : Cytokine markers were found to be increased in posttraumatic brain tissue. Malondialdehyde and glutathione reductase levels were lower in group 3 compared to group 2. In addition, superoxide dismutase, glutathione peroxidase and catalase levels were significantly higher in group 3 compared to group 2. In histological evaluation, congestion in the piamater layer, cell infiltration, vascular congestion, hemorrhage and neuronal degeneration were significantly decreased in group 3 compared to group 2. DXP seems to be beneficial in neurological recovery in terms of histological and oxidative changes after head trauma in rats. Conclusion : DXP should be further evaluated for its possible therapeutic effect in TBI.

Objective: : Dexpanthenol (DXP), which has known neuroprotective effects, has been shown to be beneficial in various experimental models and ischaemic diseases. The aim of this study was to investigate the possible neuroprotective effects of DXP in a traumatic brain injury (TBI) model. Methods: : Thirty-six Wistar-Albino female rats, approximately 6 months old, weighing 220–285 g were used. All rats were subjected to closed head trauma by dropping a weight of 350 g on the parietal region from a height of 50 cm at an angle of 180 degrees in the prepared head trauma model setup. The rats were divided into four groups as control (group 1), trauma (group 2), trauma + DXP (group 3), and DXP (group 4). In group 3, DXP was administered intraperitoneally at a dose of 500 mg/kg for six times at 30 minutes, 6, 12, 24, 36, and 48 hours. In group 4, DXP was administered intraperitoneally simultaneously with group 3 without causing head trauma. Blood samples were taken from all rats 72 hours later for biochemical examination. After blood samples were taken, rats were decapitated under general anaesthesia. Cerebral tissue samples were taken from decapitated rats for immunohistochemical and histopathological examination. Results: : Cytokine markers were found to be increased in posttraumatic brain tissue. Malondialdehyde and glutathione reductase levels were lower in group 3 compared to group 2. In addition, superoxide dismutase, glutathione peroxidase and catalase levels were significantly higher in group 3 compared to group 2. In histological evaluation, congestion in the piamater layer, cell infiltration, vascular congestion, hemorrhage and neuronal degeneration were significantly decreased in group 3 compared to group 2. DXP seems to be beneficial in neurological recovery in terms of histological and oxidative changes after head trauma in rats. Conclusion : DXP should be further evaluated for its possible therapeutic effect in TBI.

BACKGROUND AND OBJECTIVES: QRS complex fragmentations are frequently seen on routine electrocardiograms with narrow or wide QRS complex. Fragmented QRS complex (fQRS) is associated with increased morbidity and mortality, sudden cardiac death and recurrent cardiovascular events. In this study, we aimed to interrogate the relationship of systemic inflammation with the presence of fQRS in patients with acute coronary syndromes (ACS). SUBJECTS AND METHODS: Two-hundred and twenty eligible patients with ACS that underwent coronary angiography were enrolled consecutively in this study. Patients with significant organic valve disease and those with any QRS morphology that had a QRS duration > or =120 ms as well as patients with permanent pacemakers were excluded from this study. RESULTS: Patients with fQRS were of a higher age (p=0.02), had increased C-reactive protein (CRP) levels (p<0.001), prolonged QRS time (p<0.001), extent of coronary artery disease (CAD) (p<0.001), creatine kinase-MB (CK-MB) levels (p=0.006) and Q wave on admission electrocardiography (p<0.001) in comparison to patients with non-fragmented QRS. When we performed multiple logistic regression analysis, fQRS was found to be related to increased CRP levels {odds ratio (OR): 1.2, 95% confidence interval (CI): 1.045-1.316, p=0.007}, QRS duration (OR: 1.1, 95% CI: 1.033-1.098, p<0.001), extent of CAD (OR: 1.5, 95% CI: 1.023-2.144, p=0.037), Q wave (OR: 2.2, 95% CI: 1.084-4.598, p=0.03) and CK-MB levels (OR: 1.0, 95% CI: 1.001-1.037, p=0.04) independently. CONCLUSION: In our study, we found that fQRS was independently related to increased CRP. Fragmented QRS that may result as an end effect of inflammation at cellular level can represent increased cardiac risk by different causative mechanisms in patients with ACS.
Acute Coronary Syndrome ; C-Reactive Protein ; Coronary Angiography ; Coronary Artery Disease ; Creatine ; Death, Sudden, Cardiac ; Electrocardiography ; Humans ; Inflammation ; Logistic Models ; Risk Assessment

OBJECTIVE: Purinergic 2X7 receptor (P2X7R) activation is known to be involved in pathogenesis of depression. Our aims were to investigate P2X7R-activated inflammasome pathways in parallel with induction of depression and to test the antidepressant-like effects of the selective P2X7R antagonist Brilliant Blue G (BBG) in a rat model of chronic unpredictable mild stress (CUMS). METHODS: Male Wistar albino rats were divided into control, CUMS, CUMS+BBG25 (25 mg/kg/day) and CUMS+BBG50 (50 mg/kg/day) groups (n=10 for each group). Various stressors were applied to rats for 6 weeks to establish the CUMS model and daily BBG treatment was started at the end of 3rd week. Sucrose preference test and forced swim test (FST) were performed to assess antidepressant-like effects. Brain samples were obtained for real-time polymerase chain reaction and immunohistochemistry analysis. RESULTS: In FST, duration of immobility was reduced in the CUMS+BBG50 group. Also, BBG treatment significantly enhanced sucrose preference. While NLRP3 gene expression levels were unchanged in rats exposed to the CUMS protocol, expression levels of other inflammasome pathway factors NLRP1, caspase-1, ASC, NF-κB, IL-1β, IL-6 and P2X7R were increased. BBG treatment reduced expression levels of these factors. Likewise, Iba-1 and GFAP immunoreactivities were enhanced by the CUMS protocol and this action was reversed by BBG treatment. CONCLUSION: Chronic administration of BBG in CUMS model results in antidepressant-like activity in a dose dependent manner. Molecular and histological results show that these effects might be at least partially related to the suppression of inflammasome-related neuroinflammatory responses and suggest involvement of NLRP1 in depression.
Animals ; Brain ; Depression ; Gene Expression ; Humans ; Immunohistochemistry ; Inflammasomes ; Interleukin-6 ; Male ; Models, Animal ; Rats ; Real-Time Polymerase Chain Reaction ; Receptors, Purinergic P2 ; Receptors, Purinergic P2X7 ; Sucrose