Cognitive function in Meniere's disease.

Meniere's disease is an otological disease characterized by various symptoms that include episodic peripheral vertigo, sensorineural hearing loss, tinnitus, and aural fullness, all of which deteriorate the maintenance of daily activities. We aimed to investigate cognitive function in Meniere's disease patients and compare their results to those of healthy controls. Eighteen patients diagnosed with definite Meniere's disease without any psychiatric, neurological or otological comorbidity, and 30 healthy controls with normal cognitive functions were included in the study. General cognitive status, attention, verbal memory, visual memory, executive and visuospatial function were measured by detailed neuropsychological tests in both groups. In the patients with Meniere's disease, pure-tone hearing thresholds, and speech discrimination scores were also measured. Patients with Meniere's disease showed lower levels of performance in the trail making test, Oktem verbal memory processes, Rey Complex Figure Test, Wisconsin Card Sorting Test, semantic and phonemic fluency than did healthy controls. In other words, there were deficits in attention, recognition and recall in verbal memory, recall in visual memory, visual spatial construction, and planning skills in patients with Meniere's disease. Education years and depression scores of participants had a significant effect on cognitive function in all groups. This study is an update and confirmation of the findings of studies showing cognitive impairment in patients with Meniere's disease. In addition to previous findings, this study found a decrease in executive function performance in patients with Meniere's disease compared to healthy controls. Unlike previous studies, this study comprehensively addressed all cognitive functions and included a control group. Our results emphasize that executive functions, which are high-level cognitive processes, may affect the compliance of patients with Meniere's disease treatment and follow-up processes.

Wide-Band Tympanometry Results during an Acute Episode of Ménière's Disease.

BACKGROUND: Wide-band tympanometry (WBT) was introduced as a beneficial diagnostic test for Ménière's disease (MD) almost 15 years ago. However, an acute episode of MD has not been evaluated by using WBT yet. OBJECTIVE: To investigate WBT findings in patients with MD during acute attacks. METHOD: Thirty definite MD patients with unilateral acute low-tone sensorineural hearing loss and aural fullness, and thirty age- and sex-matched control subjects were enrolled prospectively in a tertiary referral center. Ears were divided into three groups as follows: (1) affected ears of MD patients, (2) contralateral ears of MD patients, (3) control ears. Individuals underwent WBT. The resonance frequency (RF), mean absorbance value, mean low- and high-frequency absorbance values (LF-A and HF-A), and double peak width at 2 kHz of conductance tympanometry (2-kHz PW) were assessed. RESULTS: Seventy percent in group 1, 66.7% in group 2, and 78.3% in group 3 demonstrated double peaks at 2 kHz. The mean 2-kHz PW values were 157.52 ± 79.19, 177.40 ± 79.14, and 139.64 ± 87.501 daPa for groups 1, 2, and 3, respectively. There were no significant differences between groups with respect to 2-kHz PW, RF, absorbance, LF-A, and HF-A. CONCLUSION: This was the first study that evaluated the effects of acute Ménière attacks on WBT findings. An acute Ménière attack was found to have no significant effect on the 2-kHz PW and other variables measured using WBT.

Favourable effect of ß-glucan treatment against cisplatin-induced reproductive system damage in male rats.

The aim of this study was to investigate the potential beneficial effects of ß-glucan treatment against oxidative, histological and spermatological damage caused by cisplatin on the male reproductive system. Twenty-eight Sprague Dawley male rats were used in the study. The rats were randomly divided into four equal-sized groups: a control group, cisplatin group (7 mg/kg in a single-dose cisplatin administered intraperitoneally), ß-glucan group (ß-glucan given at a dose of 50 mg kg-1  d-1 for 14 day) and a cisplatin plus ß-glucan group (cisplatin and ß-glucan administered together at the same dose). Cisplatin administration induced an increase in the level of thiobarbituric acid-reactive substances, a lipid peroxidation indicator. It induced a decrease in enzymatic (superoxide dismutase, catalase and glutathione peroxidase) activities and nonenzymatic (reduced glutathione) antioxidant levels. In addition, cisplatin caused both histological and spermatological damage, as shown by a decrease in sperm motility and epididymal sperm concentrations and an increase in abnormal sperm rates. The ß-glucan treatment improved cisplatin-induced oxidative, histological and spermatological damage. This study revealed that ß-glucan treatment provided prevention against male reproductive system damage caused by cisplatin. These preventative effects were likely due to its antioxidant properties.

Turkish validation of the Sino-Nasal Outcome Test-22.

OBJECTIVES: The Sino-Nasal Outcome Test (SNOT)-22 is a widely used health-related quality of life questionnaire. This study aimed to conduct a translation and validation study of the SNOT-22 in the Turkish language. DESIGN: We achieved a convenient translation and cultural adaptation process to translate the original SNOT-22 into the Turkish language (observational prospective cohort study). SETTING: This study was conducted in a single tertiary-level university hospital. PARTICIPANTS: We performed reliability, validity and responsiveness analyses in 313 participants. One hundred eighty-nine of the participants were the chronic rhinosinusitis (CRS) group, and 79 healthy volunteers enrolled in the control group. Twenty-nine participants who underwent endoscopic sinus surgery for CRS were evaluated for pre-postoperative responsiveness analysis. MAIN OUTCOME MEASURES: Reliability (internal consistency and test-retest reproducibility), validity, responsiveness, sensitivity and specificity. RESULTS: The internal consistency coefficient (Cronbach's alpha) was 0.909 in the CRS test group, 0.955 in the CRS retest group, and 0.916 in the control group. The reliability value (Pearson correlation coefficient) of the test-retest group was 0.901. The validity was assessed by the independent sample t-test between the CRS and control groups and resulted in a significant difference (P < 0.001). Responsiveness was interpreted using the paired t-test between pre- and post-medical and pre- and post-surgical treatment groups; statistical analysis found significance in both groups (P < 0.001). When using the SNOT-22 cut-off value of 33.5, the sensitivity and specificity of the Turkish version of the SNOT-22 was 54.5% and 75.9%, respectively (95% CI, area under the curve (AUC): 0.69, range 0.624â€"0.756, P = 0.000). CONCLUSIONS: The authors suggest that the Turkish SNOT-22 is a valid, reliable, reproducible and responsive questionnaire.

Protective and therapeutic effects of dexpanthenol on isoproterenol-induced cardiac damage in rats.

The purpose of the study was to explore the protective and therapeutic effects of dexpanthenol (DEX) on isoproterenol (ISO)-induced cardiac damage. Forty rats were distributed into four groups: group I (Control); group II (ISO); ISO (150 mg/kg/day) was given to rats once a day for 2 consecutive days with an interval of 24 h; group III (DEX+ISO): DEX (250 mg/kg) was applied 30 min before the first ISO administration and continued in the next two days after second ISO administration; group IV (ISO+DEX): After the ISO treatment at 1st and 2nd days, DEX was given at 3rd and 4th days. Rats were monitored for mean arterial blood pressure (BP), heart rate, oxygen saturation (%SO2 ), and electrocardiography (ECG). Heart tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), reduced glutathione (GSH), total oxidant status (TOS); total antioxidant capacity (TAC), oxidative stress index (OSI), and caspase-3 were determined. BP and SO2 values indicated a significant decrease in the ISO group. Also, T wave negativity was observed in 6 of 10 rats, SOD, CAT, and GPX levels were significantly lower in ISO group than control group. ISO administration increased TOS and OSI levels, whereas DEX treatment significantly reduced these parameters. Also, ISO-induced morphological alterations such as disorganization of cardiomyocytes, loss of myofibrils and cytoplasmic vacuolization whereas these histological damages were significantly decreased in ISO+DEX and DEX+ISO groups when compared to the ISO group. This study implies the cardioprotective effects of DEX on ISO-induced cardiotoxicity.

The beneficial effects of nerolidol and hesperidin on surgically induced endometriosis in a rat model.

The objective of this article is to analyze the effects of nerolidol and hesperidin treatment on surgically induced endometriosis in a rat model. Endometriosis was induced in 24 healthy adult female Wistar albino rats via homologous uterine horn transplantation. Three operations were performed on each rat. After the second operation, the rats were randomized into control, nerolidol, and hesperidin treatment groups, and medications were administered for 2 weeks. The effects of the drugs on the endometriotic foci were evaluated after the third operation. Compared with the endometriosis control group, the average volume of the lesions was significantly lower in rats treated with hesperidin and nerolidol. Malondialdehyde levels were significantly reduced in the nerolidol-treated group, and glutathione levels and superoxide dismutase activity were significantly elevated in the endometriotic foci of both the hesperidin- and nerolidol-treated groups compared with the endometriosis group. Hesperidin and nerolidol treatment also improved histological parameters, such as hemorrhage, vascular congestion, necrosis, and inflammatory cell infiltration in the endometriotic foci. The results of this study demonstrated that treatment with the potent antioxidants nerolidol and hesperidin caused a significant regression of surgically induced endometriotic foci in rats.

Resveratrol reduces light and electron microscopic changes in acetaminophen-induced hepatotoxicity in rats: Role of iNOS expression.

INTRODUCTION: Hepatotoxicity is a major complication of acetaminophen (APAP), a widely used analgesic and antipyretic drug. Resveratrol (RSV) is a naturally occurring diphenol and it has anticancer, antioxidant, and anti-inflammatory properties. OBJECTIVES: In this study, the beneficial effects of RSV on APAP-induced hepatotoxicity was investigated in rats. MATERIALS AND METHODS: Group 1: Ethanol, Group 2: Saline, Group 3: RSV (10 mg/kg/ip), Group 4: APAP (1000 mg/kg/ip/single dose), Group 5: APAP+RSV (20 min after administration of APAP). The rats were sacrificed 24 h after administration of APAP. Light and electron microscopic changes were evaluated. Levels of malondialdehyde (MDA) and glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities were determined in liver tissue. RESULTS: Rats of the ethanol, saline, and RSV groups did not present any histopathological alterations. In the APAP group, we observed vascular congestion, necrosis, inflammation, sinusoidal dilatation, and loss of glycogen content. In the APAP+RSV group, these changes were markedly reduced. iNOS immunostaining showed very weak positive stained hepatocytes the sections of control, saline, and RSV groups. However, in the APAP group, iNOS immunostaining was most evident in pericentral hepatocytes. In the same areas in APAP+RSV group, intensity of iNOS immunostaining decreased. A significant increase in MDA and decreases in GSH level, CAT, and SOD activity indicated that APAP-induced hepatotoxicity was mediated through oxidative stress. Significant beneficial changes were noted in tissue oxidative stress indicators in rats treated with RSV. CONCLUSION: These biochemical, histopathological, and ultrastructural findings revealed that RSV reduced the severity of APAP-induced alterations in liver.

The protective effect of fish oil against cisplatin induced eye damage in rats.

Ocular toxicity induced by anticancer chemotherapy is not uncommon, but underestimated and under-reported. Visual changes have been attributed to a number of chemotherapeutic agents in humans. Cisplatin (CP), a heavy metal compound, is used in the treatment of many types of tumours. CP is known to produce nonspecific blurred vision, papilledema, and optic neuritis for high doses as well as cumulative dose regimens. The aim of this study was to investigate the possible beneficial effects of fish oil (FO) on eye tissue oxidative status and histological alterations against CP-induced in the rats. The animals were randomly divided into the following four groups: the control, CP, FO, and CP + FO groups. CP was intraperitoneally administered at the dose of 7 mg/kg and FO was orally given at 1 softgel per day for 14 days. The eye injury was assessed by biochemical and histological examinations. The levels of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were evaluated in the eye tissue. TBARS levels were significantly higher, the activities of the antioxidant enzyme and GSH levels were significantly lower in the CP group than in the control group. The histopathological evaluation also confirmed the foregoing findings. On the other hand, treatment of FO ameliorated the biochemical and histological alterations caused by CP. The results showed that treatment with FO may protect against the negative ocular effects of CP.

Anti-inflammatory Montelukast prevents toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin: Oxidative stress, histological alterations in liver, and serum cytokine levels.

This study aimed to investigate the potential beneficial effects of the montelukast (ML) on oxidative stress and histological alterations in liver tissues and cytokine levels in rats intoxicated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Rats were divided randomly into four equal groups (control, TCDD, ML, TCDD + ML). TCDD were administered by gavages dissolved in corn oil at the doses of 2 µg/kg/week, and ML was given intraperitoneally at the dose of 10 mg/kg/day. Oxidative status, histological alterations, and cytokine levels were analyzed on day 60. The results showed that although TCDD induced oxidative stress via significant increase in formation of thiobarbituric acid reactive substance, it caused a significant decline in glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) levels in liver. Besides, TCDD led to significant histopathological damage in liver and serum cytokine levels alterations (increase in tumor necrosis factor α and interleukin 1ß levels). In contrast, ML treatment reversed oxidative effects of TCDD by increasing the levels of GSH, CAT, and SOD and decreasing the formation of TBARS. Also, it can normalize the levels of histological and cytokine alterations induced by TCDD. In conclusion, it was determined that TCDD exposure caused adverse effects on cytokine levels, histological alterations, and oxidative stress in rats. However, ML treatment partially eliminated toxic effects of TCDD. Thus, it was judged that coadministration of ML with TCDD may be useful to attenuate the negative effects of TCDD.

Toxic effects of systemic cisplatin on rat eyes and the protective effect of hesperidin against this toxicity.

CONTEXT: In the present study, cisplatin (CP) induced eye toxicity and the beneficial effect of hesperidin (HP) was investigated. METHODS: Twenty-eight rats were equally divided into four groups; the first group was kept as control. In the second and third group, CP and HP were given at the doses of 7 mg/kg and 50 mg/kg/d, respectively. In the fourth group, CP and HP were given together at the same doses. Tissue samples were collected on day 14 of CP treatment. RESULTS: The results demonstrated that CP caused a significant increase in thiobarbituric acid reactive substances (TBARS) levels and decrease of glutathione levels and antioxidant enzyme activity (catalase, superoxide dismutase and glutathione peroxidase) in eye tissues compared to other groups, HP prevented these effects of CP. Besides, CP led to histopathological damage in the retina and cornea. On the other hand, HP treatment prevented histopathological effects of CP. CONCLUSION: CP had severe dose-limiting toxic effects and HP treatment can be beneficial against the toxic ocular effects of CP. Thus, it appears that co-administration of HP with CP may be a useful approach to attenuate the negative effects of CP on the eye.

Hesperidin, a Citrus Flavonoid, Has the Ameliorative Effects Against Experimental Autoimmune Encephalomyelitis (EAE) in a C57BL/J6 Mouse Model.

The aim of this study was determined the effects of Hesperidin (HP) on neuronal damage in brain tissue caused by Experimental allergic encephalomyelitis (EAE), an established model of multiple sclerosis in C57BL/J6 mice. To explore 40 mice were equally divided into four groups: (1) Control, (2) EAE, (3) HP, and (4) HP + EAE. 14 days after induction of EAE with MOG35-55 and pertussis toxin, the mice treated with HP at the doses of 50 mg/kg/day for 7 days subcutaneously. To our results HP treatment prevents the oxidative stress caused by EAE via a decrease in lipid peroxidations and increase in elements of the antioxidant defense systems in brain tissue. Also, EAE elevate the IL-17, express the pro-inflammatory cytokines, and caspase-3-like immunreactivity, show apoptosis, staining in EAE mice brain and increased the incidence of histopathological damage. However, immonohistochemical and histological changes were reversed with HP. Moreover, elevated TNF-α and IL-1ß levels, a result of EAE, were decreased in serum and neurological deficits as clinical signs were reversed with HP treatment in EAE mice, given HP. In conclusion, HP treatment effectively prevents oxidative, immunological and histological damage in the brain caused by EAE. It was thought that the beneficial effects of HP are likely a result of its strong antioxidant and anti-inflammatory properties.

Hesperidin protects brain and sciatic nerve tissues against cisplatin-induced oxidative, histological and electromyographical side effects in rats.

In the present study, the beneficial effect of hesperidin (HP), a citrus flavonoid, on cisplatin (CP)-induced neurotoxicity was investigated. A total of 28 rats were equally divided into four groups; the first group was kept as control. In the second and third groups, CP and HP were given at the doses of 7 and 50 mg/kg/day, respectively. In the fourth group, CP and HP were given together at the same doses. The results indicated that although CP caused significant induction of lipid peroxidations and reduction in the antioxidant defense system potency in the brain and sciatic nerve, HP prevented these effects of CP. Besides, CP led to histopathological damage, mainly apoptosis, as well as electromyographical (EMG) changes in sciatic nerve. On the other hand, HP treatment reversed histopathological and EMG effects of CP. In conclusion, CP had severe dose-limiting neurotoxic effects and these effects of CP can be prevented by HP treatment. Thus, it appears that coadministration of HP with CP may be a useful approach to attenuate the negative effects of CP on the nervous system.

Neuroprotective effects of ß-myrcene following global cerebral ischemia/reperfusion-mediated oxidative and neuronal damage in a C57BL/J6 mouse.

The aim of this study was to investigate the effects of ß-myrcene (MYR) on oxidative and histological damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. Mice (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) MYR, and (4) MYR + I/R. The SH group was used as a control and received 0.1 % carboxymethyl cellulose (CMC) as a vehicle following a medial incision without carotid occlusion. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and treated with the vehicle intraperitoneally (i.p.) for 10 days. In the MYR group, mice were given 200 mg/kg MYR dissolved in 0.1 % CMC for 10 days following a medial incision without carotid occlusion. In the MYR + I/R group, the I/R procedure was performed exactly as in the I/R group, and they were then treated with the same dose of MYR for 10 days. Cerebral I/R induced oxidative stress via an increase in thiobarbituric acid reactive substances (TBARS) formation and a decrease in the antioxidant defense systems, including glutathione (GSH), catalase, glutathione peroxidase (GPx) and superoxide dismutase (SOD). However, MYR treatment protected against the oxidative effects of I/R by inducing significant increases in GSH, GPx, and SOD and a significant decrease in the formation of TBARS. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by MYR treatment. This study has demonstrated that MYR effectively attenuates oxidative and histological damage in the brain caused by global I/R. The beneficial effects of MYR probably contribute to its strong antioxidant and radical scavenging properties. In conclusion, MYR may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, may be a viable and safe alternative treatment for ischemic stroke in humans.

Protective effects of melatonin and quercetin on experimental lung injury induced by carbon tetrachloride in rats.

INTRODUCTION: Exposure to carbon tetrachloride (CCl4), a well-known toxicant, causes tissue damage by inducing oxidative stress via formation of free radicals. The fundamental structure of the organs of rats and humans is similar, so administration of CCl4 to rats is an accepted experimental model to produce oxidative damage to various tissues including pulmonary tissue. In this study, we evaluated the protective capacity of melatonin and quercetin against CCl4-induced oxidative lung damage in rats. MATERIAL-METHODS: Rats were divided into five groups each containing seven rats as follows: Control group, Olive oil group CCl4 group, CCl4+Melatonin, and CCl4+Quercetin group. The tissue samples were processed by routine histological and biochemical procedures. Sections were stained with Hematoxylin-eosin and Masson's trichrome. Histopathologic damage score was calculated. Malondialdehyde (MDA) and glutathione (GSH) levels and catalase (CAT) activities were assayed. RESULTS: The lung sections of control groups showed normal histological characteristics. Fibrosis, interstitial hemorrhage, epithelial desquamation in bronchiole and alveoli, intra-alveolar edema, leukocyte, and macrophage infiltration were observed in lung sections of rats exposed to CCl4 alone. The findings were reduced in the treatments groups. The MDA level in the CCI4 group were significantly higher than in the other groups (p < .001), and the CAT and GSH levels in the CCI4+Mel and CCI4+Quer groups were significantly higher than in the CCI4 group (p < .05). CONCLUSION: In conclusion, we suggest that agents with antioxidant properties such as melatonin and quercetin may have positive effects in the treatment of pulmonary diseases characterized by especially edema, inflammation, and fibrosis.

Fish oil protects the peripheral and central nervous systems against cisplatin-induced neurotoxicity.

OBJECTIVE: The protective effects of fish oil (FO) on cisplatin (CP)-induced central and peripheral neurotoxicity were investigated in rats. METHODS: Rats (n = 28) were divided equally into four groups, the first group was kept as a control. In the second and third groups, CP and FO were given at doses of 7 mg/kg and 1 softgel/rat/day, respectively. In the fourth group, CP and FO were given together at the same doses. RESULTS: Although CP caused significant oxidative damage, via induction of lipid peroxidation and reduction in the antioxidant defense system potency, FO treatment largely reversed these effects. CP also resulted in histopathological damage, such as apoptosis, and electromyographical changes in the sciatic nerve. FO treatment partially prevented the histopathological and electromyographical effects of CP. DISCUSSION: CP has severe central and peripheral neurotoxic effects in rats and these effects were largely prevented by FO treatment. Thus, it appears that co-administration of FO with CP may be a useful approach to attenuate the negative effects of CP on the nervous system.

Hesperidin attenuates oxidative and neuronal damage caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model.

The aim of this study was to determine the effects of hesperidin (HP) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. For this purpose, a total of 40 mice were divided equally into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) HP, and (4) HP+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with vehicle for 10 days. In the HP group, mice were administered HP (100 mg/kg) for 10 days without carotid occlusion. In the HP+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with 100 mg/kg HP for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidation and a decrease in the components of the antioxidant defense system. Furthermore, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue. HP treatment significantly reversed the oxidative effects of I/R and inhibited the development of neurodegenerative histopathology. Therefore, the current study demonstrates that HP treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, the beneficial effects of HP are likely a result of its strong antioxidant and free radical-scavenging properties. HP may be an useful treatment to attenuate the negative effects of global cerebral I/R.

The beneficial effects of 18ß-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model.

This study investigated the effects of 18ß-glycyrrhetinic acid (GA) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. All subjects (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) I/R, (3) GA, and (4) GA+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with the vehicle for 10 days. In the GA group, mice were given GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the GA+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with the same dose of GA for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidaitons and a decrease in elements of the antioxidant defense systems. However, GA treatment was protective against the oxidative effects of I/R by inducing significant increases in antioxidant defense systems and a significant decrease of lipid peroxidations. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by GA treatment. Therefore, the current study demonstrated that GA treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, GA may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, it may be a viable and safe alternative treatment for ischemic stroke in humans.

Methotrexate for recurrent chronic rhinosinusitis with nasal polyps: A randomized, controlled, phase 2 clinical trial.

OBJECTIVE: This randomized, controlled, open-label, phase 2 clinical trial aimed to assess the efficacy and safety of low-dose methotrexate as maintenance therapy for recurrent postoperative chronic rhinosinusitis with nasal polyps (CRSwNPs). METHODS: Forty-one patients with CRSwNPs who experienced postoperative polyp recurrence(s) were randomly divided into three groups to receive one of the following treatments for 8 weeks: daily intranasal mometasone furoate monohydrate 200 mcg (control [intranasal corticosteroids (INCS)] arm, n = 13]); daily per oral methylprednisolone 8 mg (oral corticosteroids [OCS] arm, n = 14); and once weekly per oral 10 mg methotrexate (MTX arm, n = 14). All patients were assessed at three clinical visits according to the Lund-Kennedy endoscopic grading system (LKES), visual analog scale (VAS), Turkish version of the Sinonasal Outcome Test-22 (SNOT-22), peak nasal inspiratory flow (PNIF), butanol olfactory threshold test (BuOT), serum total IgE level, presence of peripheral eosinophilia, serum biochemical assays, and adverse events. RESULTS: All efficacy outcome measures significantly improved in all three groups, except for the nonrecovery of peripheral eosinophilia in the INCS group. There was no significant difference among the groups in terms of LKES scores. Scores for the Turkish version of the SNOT-22, PNIF, BuOT, and serum IgE levels were also similar among the groups. However, total VAS scores recovered significantly better in the INCS group than in the MTX group. Serum biochemical assays remained normal in all groups. Adverse events were minor and observed only in the OCS group. CONCLUSION: Low-dose MTX was a safe and effective maintenance therapy for patients with recurrent postoperative CRSwNPs.

Effects of Cross-linked Hyaluronic Acid in a Rat Model of Vestibular and Cochlear Toxicity.

Objective: To investigate the effects of cross-linked hyaluronic acid (CLHA) in an experimental model of vestibulotoxicity and cochleotoxicity. Methods: Twenty-eight female Wistar albino rats (200-250 g) were divided into four groups. Group A received 0.06 mL of 13.33 mg/mL gentamicin, Group B received 0.06 mL of CLHA, Group C received 0.03 mL of 26.66 mg/mL gentamicin and 0.03 mL CLHA, and Group D received 0.06 mL of 0.09% saline. All groups underwent auditory brainstem response testing at 4-32 kHz, signal-to-noise ratio of distortion product otoacoustic emission measurements at 1.5-8 kHz and vestibular tests on days 0,1,7,10. The rats were sacrificed, and their labyrinths were histologically assessed and scored. Results: The hearing thresholds of Groups A and C were similar and significantly higher than those of the other groups at all frequencies, beginning from day 1. The vestibular and histological scores of Groups A and C were similar and significantly higher than those of the other groups from day 1. The audiological results, vestibular scores, and histological scores of Groups B and D were similar, except for a temporary middle ear effusion and hearing threshold shift in Group B. No significant deterioration was observed in the audiological, vestibular, and histological analyses of Groups B and D. Conclusion: That both Group A and Group C similarly showed worsening audiological, vestibular, and histological tests suggests that CLHA did not alter the pharmacokinetics and histologic results of gentamicin.

Beneficial effects of montelukast against cisplatin-induced acute renal damage in rats.

OBJECTIVE: In this study, the therapeutic and protective effects of montelukast against cisplatin (CP)-induced acute renal damage were investigated. MATERIALS AND METHODS: Thirty-five female rats were divided into five groups as follows: (1) control, (2) montelukast (10 mg/kg daily for 10 days per-oral (p.o.), (3) CP (single dose 7 mg/kg intraperitoneally (i.p.)), (4) CP + montelukast (10 mg/kg daily for 10 days p.o., after 3 days of the injection of CP), (5) montelukast (10 mg/kg daily for 10 days p.o.) + CP (single dose 7 mg/kg i.p., after the last dose of montelukast). At the end of the experiment, malondialdehyde (MDA), a lipid peroxidation product, myeloperoxidase (MPO), and reduced glutathione (GSH) levels were determined in the renal tissue. Also, blood urea nitrogen (BUN) and creatinine (Cr) levels were assayed from the trunk blood samples. RESULTS: CP treatment caused a significant elevation of MDA, MPO, BUN, and Cr levels when compared with the control group. Also, GSH levels were found to be reduced due to the CP treatment. Montelukast administration after CP injection ameliorated all of these parameters. Our histopathological findings (marked swelling of epithelial cells, tubular dilatation, tubular desquamation, and loss of brush border in the kidney) were consistent with the biochemical results. CONCLUSION: Montelukast treatment after CP injection exerted therapeutic effects against CP-induced acute kidney damage.