Pre- and post-surgery treatments in rectal cancer: a long-term single-centre experience.

BACKGROUND: Our study evaluated long-term survival outcomes in rectal cancer patients treated with preoperative radiotherapy, and the impact on survival of concomitant and postoperative adjuvant chemotherapy (ctx), among other prognostic factors. METHODS: The study included 196 patients [median age: 58 years (range: 20-86 years); 63.0% men] with locally advanced rectal carcinoma and, in some cases, resectable liver metastasis. Rates of distant metastasis and local recurrence and of 5-year distant metastasis-free survival (dmfs) and overall survival (os) were determined. RESULTS: The 5-year os rate was 57.0%, with a median duration of 81.5 months (95% confidence interval: 73.7 months to 89.4 months), and the 5-year dmfs rate was 54.1%, with a median duration of 68.4 months (95% confidence interval: 40.4 months to 96.4 months). Prognostic factors for higher os and dmfs rates were downstaging (p = 0.013 and p = 0.005 respectively), radiotherapy dose (50 Gy vs. 56 Gy or 45-46 Gy, both p = 0.002), and concomitant ctx use (p = 0.004 and p = 0.001) and type (5-fluorouracil-leucovorin-folinic acid vs. tegafur-folinic acid, p = 0.034 and p = 0.043). Adjuvant ctx after neoadjuvant long-term concomitant chemoradiotherapy (ccrt) and surgery was associated with better 5-year os rates for postoperative T0-T3 disease (p = 0.003) and disease at all lymph node stages (p = 0.001). CONCLUSIONS: Our findings revealed a favourable survival outcome with long-term fractionated irradiation and concomitant 5-fluorouracil-based ctx, achieving 5-year os and dmfs rates of 57.0% and 54.1% respectively. Preoperative administration of radiotherapy (50 Gy) and postoperative adjuvant ctx were associated with a significant survival benefit. Radiation doses above 50 Gy and the interval between ccrt and surgery had no significant effect on survival.

Protective role of methylprednisolone and heparin in ischaemic-reperfusion injury of the rat testicle.

This study evaluated the therapeutic efficacy of heparin and methylprednisolone in the treatment of ischaemic reperfusion (IR) injury of the testis. Twenty-four male Sprague-Dawley rats were allocated equally into three groups of eight animals each. The left testes were rotated 720° for 2 h in the rats in the torsion-detorsion group. Rats in the treatment groups underwent the same surgical procedure as the torsion-detorsion group but were also given methylprednisolone (group II) or heparin (group III) by an intraperitoneal route 30 min prior to detorsion. Left orchiectomy was performed in all rats from each experimental animal at 2 h after detorsion, and the tissue was harvested for the measurement of malondialdehyde (MDA), protein carbonyl (PC) and nitric oxide (NO) and the endogenous antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase. Additional tissue was evaluated using histopathological and immunohistochemical changes. PC and MDA levels were significantly reduced in the treated groups compared to the control group. There was no statistically significant difference in NO level or SOD, GSH-Px and catalase activity among the treatment groups. Histopathological and immunohistochemical findings supported biochemical changes. It is concluded that pre-treatment with methylprednisolone or heparin protects the testis in ischaemic reperfusion injury caused by testicular torsion-detorsion.

Traditional risk factors and angiotensin-converting enzyme insertion/deletion gene polymorphism in coronary artery disease.

We investigated whether the insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene and serum ACE levels are associated with traditional risk factors of coronary artery disease (CAD). We enrolled 250 individuals without CAD and 750 individuals suffering from CAD who were angiographically diagnosed. Biochemical risk factors, the ACE (I/D) gene polymorphism, and ACE serum levels were compared. ACE genotypes were determined using real-time polymerase chain reaction. ACE serum levels were determined using an enzyme-linked immunosorbent assay. Lipid parameters were determined spectrophotometrically using an autoanalyzer. Compared to the control group, the CAD group showed significantly higher serum ACE levels (P < 0.001). The highest ACE levels were found in those with the DD genotype. Other genotypes also presented statistically significant differences. We observed a significant difference between the control and coronary patient groups regarding the levels of total cholesterol, triglyceride, high-density lipoprotein-cholesterol, and low-density lipoprotein-cholesterol (P < 0.05). ACE (I/D) genotypes and serum ACE levels may be associated with risk factors and the development of CAD.

Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients.

Celiac disease (CD) is a multifactorial, inflammatory small bowel disorder characterized by nutrient malabsorption resulting from mucosal damage, the latter induced by cereal products like barley, oat, and wheat. Oxidative stress has previously been reported to play an important role in the pathogenesis of CD. In the present study, we aimed to evaluate the frequency of polymorphisms that affects the structure of the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), with levels being dependent on the amount of oxidative stress and whether or not there is an association with the mutations DQA1*0501, DQB1*0201, and DRB1*04 that are frequently reported for CD. SOD and GSH-Px polymorphisms were investigated by real-time quantitative polymerase chain reaction in 265 cases. Of the 117 cases that had at least one of DQA1*0501, DQB1*0201, or DRB1*04, 98 (83.75%) also had SOD enzyme polymorphisms and 68 (58.12%) also had GSH-Px polymorphisms. In conclusion, although the etiology of CD is not yet entirely clear, many mechanisms have been suggested. This study supports the notion that SOD and GSH-Px polymorphisms are involved in CD development, even though our findings were not statistically significant, and, furthermore, are influenced at various levels. SOD polymorphisms and activities were more frequently identified than those of GSH-Px.

The effects of carvedilol on ischemia-reperfusion injury in the rat testis.

OBJECTIVE: To analyze the oxidative damage and histopathological alterations caused by ischemia-reperfusion (I/R) injury and ameliorative effects of carvedilol (CVD) in the rat testis. MATERIALS AND METHODS: Twenty-one male rats were randomized into 3 groups as follows: Group I (n = 7); control (sham) group, Group II (n = 7); I/R group, in which I/R injury was performed by torsing the left testis 720 ° clockwise for 2 hours and detorsing for 2 hours. Group III (n = 7); CVD treatment group; in addition to I/R process, one-dose of CVD was administered (2mg/kg, i.p) 30 min. before detorsion. Levels of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and levels of malondialdehyde (MDA) and protein carbonyl (PC) were determined in testicular tissues and serum of rats. Testicular tissues were also examined histopathologically and Johnsen scores were determined. RESULTS: Activities of SOD and GSH-Px in serum and testicular tissues were increased by I/R, but administration of CVD decreased these levels (p < 0.001 and p = 0.001). Significantly increased MDA levels in serum and testicular tissues were decreased by CVD treatment (p < 0.001 and p = 0.001). Concerning PC levels in serum and testicular tissues, there was no statistically significant difference between the groups (p = 0.989 and p = 0.428). There was not a statistically significant difference in terms of mean Johnsen scores between the groups (p = 0.161). CONCLUSIONS: Administration of CVD decreased oxidative damage biochemically in the rat testis caused by I/R injury, but histopathologically no change was observed betwe¬en all of the groups.

In vitro and in vivo effects of green-synthesized silver nanoparticles against Giardia lamblia infection.

The current experimental study is designed to examine the in vitro and in vivo effects of green synthesized silver nanoparticles (AgNPs) against Giardia lamblia, a major cause of parasitic diarrhea. The precipitation method was employed for the green synthesis of AgNPs by Astragalus ecbatanus aqueous extract. In the, in vitro, Giardia lamblia cysts and trophozoites were exposed to AgNPs at 10, 20, and 40 mg/mL for 10-360 min. The effects of AgNPs on trophozoite plasma membrane and their cytotoxic effects on normal and colon cancer cells were evaluated using Sytox green and MTT assay for cell viability. The in vivo assay included BALB/c mice, infected by Giardia, treated with AgNPs at 10, 15, and 20 mg/kg/day for one week. On the 8th day post-infection, stool examination was conducted to assess the presence of Giardia cysts and the reduction rate. The size distribution of AgNPs ranged between 5 and 80 nm, with the maximum particle size observed at 40-60 nm. AgNPs significantly (P<0.001) increased the mortality of Giardia lamblia trophozoites in a dose-dependent manner. Specifically, AgNPs at concentrations of 200 and 300 µg/mL destroyed Giardia lamblia cysts after 4 and 2 h, respectively. Trophozoites of Giardia lamblia showed more sensitivity to AgNPs compared to cysts. At concentrations of 100, 200, and 300 µg/mL, AgNPs eliminated all trophozoites after 4, 2, and 1 h of treatment, respectively. AgNPs dose-dependently reduced (P<0.001) the parasite load and viability of Giardia lamblia cysts. Exposure of Giardia lamblia trophozoites to AgNPs dose-dependently increased the plasma membrane permeability as indicated by rise in the exposed fluorescence. The CC50 value AgNPs for colon cancer and normal cell lines was 402.3 µg/mL and 819.6 µg/mL, respectively. The selectivity value greater than 2 (2.04), suggests that these AgNPs are safe for normal cells in comparison with cancer cells. This experimental study showed that AgNPs green synthesized by Astragalus ecbatanus exhibited significant in vitro and in vivo anti-Giardia activity, positioning them as potential candidates for Giardia infection treatment. Nevertheless, further research on the precise mechanisms of action and comprehensive exploration of all toxicity aspects associated with this type of AgNPs need to be considered.

Distribution of HLA-B27 and CYP2D6*4 mutations in the middle Black Sea area (Tokat) of Turkey.

We analyzed distribution of HLA-B27 and CYP2D6*4 mutations in 249 patients from Tokat province in Turkey with symptoms of arthritis, sacroiliac, joint and back pain, using a LightCycler 480 II Real-Time PCR thermal cycler. The Genes-4U was applied for studying HLA-B27 mutation, and the Tib-Molbiol commercial kit was used to examine the CYP2D6*4 mutation. Among the 249 patients, 18.5% had the HLA-B27 mutation. The CYP2D6*4 mutation was found in 22.0% (six homozygotes). Ten patients had both mutations. These frequencies are similar to what has been reported from other populations.

Serum vitamin D status and bone mineral density in fibromyalgia.

OBJECTIVES: To compare serum vitamin D levels and bone mineral density (BMD) values in patients with fibromyalgia and healthy controls. BACKGROUND: The so far available reports of low levels of vitamin D and low BMD values in patients with fibromyalgia are inconsistent. METHODS: Serum 25-hydroxyvitamin D (25-OHD) levels and BMD values were measured in thirty women with fibromyalgia and compared with thirty age-matched healthy women. Serum calcium, phosphorus, alkaline phosphatase and parathyroid hormone (PTH) levels were also measured. All participants completed the Fibromyalgia Impact Questionnaire (FIQ) and Hospital Anxiety and Depression Score (HADS). Pain severity was assessed with visual analog scale (VAS). RESULTS: Mean serum 25-OHD levels did not differ between the groups (fibromyalgia 10.57 +/- 10.46, controls 10.87 +/- 5.52 ng/l; p=0.89); nor did the frequency of vitamin D deficiency (25-OHD < or = 20 ng/l) in each group (fibromyalgia 86.7%, controls 96.7%; p=0.353). Although, mean serum PTH level was found significantly higher in fibromyalgic patients than in controls (p=0.014), only one patient and two of controls had barely elevated PTH levels. There was no relationship between vitamin D level and FIQ score (p=0.707) or HADS (p=0.824) or pain VAS (p=0.414). BMD values in the patients with fibromyalgia were comparable to those in controls at both, the lumbar spine (p=0.866) and femur neck (p=0.61). CONCLUSION: Neither vitamin D levels nor BMD values are different between women with and without fibromyalgia. In this cross-sectional study, mean serum PTH level was found higher in the fibromyalgic patients than in controls. Nevertheless, in order to confirm the findings of this preliminary study it is still necessary to perform a controlled longitudinal study (Tab. 2, Fig. 2, Ref. 35). Full Text in free PDF www.bmj.sk.

The effects of nitric oxide donor molsidomine on skeletal muscle damage in a rat hind limb model of ischemia-reperfusion.

BACKGROUND: In this experimental study, we aimed to examine the protective effect of molsidomine (MS), a nitric oxide (NO) donor, against ischemia-reperfusion (I-R) injury in a rat skeletal muscle model. METHODS: Ischemia was achieved by application of an elastic rubber band as high as possible on the left thigh of the rats. Group 1: the control group received a sham operation. Group 2: the I-R group received I-R injury to the left hind limbs. Group 3: the I-R/MS group underwent the same model of I-R injury and received MS. Group 4: the I-R/L-NAME (N-omega-nitro-L-arginine-methyl ester) group underwent the same model of I-R injury and received L-NAME, an inhibitor of NO synthase. RESULTS: In groups 2 and 4, malondialdehyde increased significantly when compared to groups 1 and 3. Superoxide dismutase, catalase and glutathione peroxidase increased significantly in group 3 compared to groups 2 and 4. The NO levels were significantly elevated in group 3 compared to groups 2 and 4. In addition, the histopathological score was considerably lower in group 3 than in group 4. The number of necrotic muscle fibers and infiltration of neutrophils were significantly reduced in the MS-treated group. CONCLUSIONS: These findings suggest that MS can exert a protective effect against skeletal muscle injury caused by I-R in the rats.

Association of plasma homocysteine and macular edema in type 2 diabetes mellitus.

PURPOSE: The aim of this study was to assess the association of macular edema (ME) with plasma homocysteine, vitamin B6, vitamin B12, and folic acid levels in patients with Type 2 diabetes. METHODS: Sixty-five diabetic subjects with no retinopathy and nonproliferative diabetic retinopathy (NPDR) (no DR, without ME, with ME: 16, 25, 24, respectively), 28 with proliferative diabetic retinopathy (PDR) (with and without ME: 14, 14, respectively), and 19 healthy subjects as control were recruited in this cross-sectional study. Plasma homocysteine, vitamin B12, vitamin B6, and folate levels were determined after 8-hour of fasting for all subjects. The levels of serum homocysteine and vitamin B6 were measured using high performance liquid chromatography (HPLC) with fluorescence detection, and the levels of serum vitamin B12 and folic acid were measured by electrochemiluminescence immunoassay. RESULTS: When diabetic groups with ME were compared with diabetic groups without ME for homocysteine, vitamin B12, vitamin B6, and folic acid, the only significant difference was detected in homocysteine levels (p=0.001). There was no significant difference between NPDR with ME group compared with NPDR without ME group and no DR group for plasma homocysteine, vitamin B12, vitamin B6, and folic acid (p=0.200, p=0.660; p=0.999, p=0.678; p=1.0, p=0.248; p=1.0, p=0.982, respectively). On the other hand, when PDR with ME group was compared with PDR without ME group, there was only significant difference in homocysteine levels (p=0.023). CONCLUSIONS: Mild to moderate elevation of homocysteine may explain the role of vascular dysregulation and endothelial dysfunction in patients with DR. The present study suggests hyperhomocysteinemia may be one of the crucial risk factors for development of ME.

Effects of caffeic acid phenethyl ester and epidermal growth factor on the development of caustic esophageal stricture in rats.

BACKGROUND/PURPOSE: An experimental study was performed to modify the healing response in caustic esophageal burns to prevent stricture development. Two different agents with different modes of actions, caffeic acid phenethyl ester (CAPE) and epidermal growth factor (EGF), were studied. CAPE has antiinflammatory, immunomodulatory, antioxidant, and antimitotic properties. EGF has known properties in supporting wound healing and in protecting esophagus from injuries. METHODS: The model described by Gehanno and its modification by Liu was used to create standard esophageal burns with 50% NaOH. The study was performed with 76 rats in 4 main groups (sham, CAPE, EGF, and control) and 2 subgroups in each for 5 and 28 days of observation. Efficacy of treatment was assessed in 28-day subgroups by measuring weight gain, contrast esophagograms on day 27, histologic evaluation by measuring stenosis index (wall thickness/lumen diameter), and collagen deposition, and biochemically by determining tissue hydroxy proline (OHP) content. RESULTS: In the end of the study, increase rates of mean body weights of the animals in the 28-day subgroups were as follows: sham, 30%; CAPE, 23%; EGF, 22%; and control, 14%. Although all the animals in subgroups significantly gained weight, the mean weight gain was significantly low in controls when compared with sham, CAPE, and EGF groups (P <.05). Contrast esophagograms on day 27 showed no stenosis in the sham, mild stenosis in CAPE and EGF, and severe stenosis with proximal dilatation in controls. Stenosis indices of the subgroups were as follows: sham, 0.29; CAPE, 0.41; EGF, 0.41; control, 0.84. Index was significantly higher in controls (P <.05). Collagen accumulation scores in the esophageal wall were as follows: Sham, 0.0; CAPE, 0.87; EGF, 0.30; control, 2.70. Scores also were significantly higher in controls (P <.05). Tissue (OHP) levels were as follows (mg/g dry tissue): Sham, 1.48; CAPE, 1.53; EGF, 1.90; control, 4.01. Production of OHP was significantly higher in controls. CONCLUSIONS: The results of the parameters in the study indicate that administration of CAPE and EGF has beneficial effects in the prevention of caustic esophageal strictures. Those effects of CAPE may occur through its antiinflammatory, immunomodulatory, and antioxidant properties, and EGF may occur through its induced proliferative properties on the esophagus.

Potential role of some oxidant/antioxidant status parameters in prefrontal cortex of rat brain in an experimental psychosis model and the protective effects of melatonin.

OBJECTIVES: The etiology of schizophrenia is unknown. However, some of the neuropathological changes in schizophrenia may be the result of increased free radical-mediated or reactive oxygen species (ROS) mediated neurotoxicity. Melatonin is a hormone produced especially at night in the pineal gland; additionally is a highly important antioxidant. The aim of this study is to indicate the contribution effect of the neuropathophysiology of schizophrenia and protective effects of melatonin against this oxidative damaged. MK-801 induced selective neurotoxicity has been proposed as an animal model for psychosis. MATERIALS AND METHODS: 21 healthy adult and male Wistar albino rats were divided into three groups. MK-801 was given intraperitoneally for 5 days in experimental psychosis group. Melatonin was given to the treatment group for 6 days by intraperitoneally. In control group, saline was given in the same way. At the 7th day of the experiments, rats were killed by decapitation. Brains were removed and prefrontal part of the brain was divided for biochemical analyses. RESULTS: Some antioxidant enzymes, malondialdehyde and protein carbonyl analyses were made by spectrophotometric methods. SOD, GSH-Px, XO activities and malondialdehyde, protein carbonyl and NO levels were found to be increased significantly in prefrontal cortex of MK-801 group (p < 0.0001) compared to the control group. In melatonin treated rats, prefrontal tissue malondialdehyde and protein carbonyl levels were decreased significantly in comparison with MK-801 group (p < 0.0001). CONCLUSIONS: MK-801 may induce oxidative stress in prefrontal cortex of rats. This experimental study provides some evidences for the protective effects of melatonin on MK-801-induced changes in prefrontal rat cortex.

Quercetin protects radiation-induced DNA damage and apoptosis in kidney and bladder tissues of rats.

Ionizing radiation (IR) can induce cell damage and cell death through the reactive oxygen species generated by radiolytic hydrolysis. The present study was aimed to determine the possible protective effects of quercetin, a well-known antioxidant agent, against IR-induced bladder and kidney damage in rats. Sprague-Dawley rats were exposed to 8-Gy whole-abdominal IR and given either vehicle or quercetin (20 mg/kg, ip). Rats were decapitated at either 36 h or 10 days following IR, where quercetin or vehicle injections were repeated once daily, and kidney and bladder samples were obtained for the determination of myeloperoxidase and caspase-3 activities, an index of tissue neutrophil infiltration and apoptosis, respectively. Radiation-induced inflammation was evaluated through tissue cytokine, TNF-α levels. In order to examine oxidative DNA damage, tissue 8-hydroxydeoxyguanosine (8-OHdG) levels were measured. All tissues were also examined microscopically. In the saline-treated irradiation groups, myeloperoxidase and caspase-3 activities, 8-OHdG and TNF-α levels were found to be increased in both tissues (p < 0.05). In the quercetin-treated-IR groups, all these oxidant responses were prevented significantly (p < 0.05). The present data demonstrate that quercetin, through its free radical scavenging and antioxidant properties, attenuates irradiation-induced oxidative organ injury, suggesting that quercetin may have a potential benefit in radiotherapy by minimizing the adverse effects and will improve patient care.

The effects of carvedilol on ischemia-reperfusion injury in the rat testis

Objective: To analyze the oxidative damage and histopathological alterations caused by ischemia-reperfusion (I/R) injury and ameliorative effects of carvedilol (CVD) in the rat testis. Materials and Methods: Twenty-one male rats were randomized into 3 groups as follows: Group I (n = 7); control (sham) group, Group II (n = 7); I/R group, in which I/R injury was performed by torsing the left testis 720º clockwise for 2 hours and detorsing for 2 hours. Group III (n = 7); CVD treatment group; in addition to I/R process, one-dose of CVD was administered (2mg/kg, i.p) 30 min. before detorsion. Levels of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and levels of malondialdehyde (MDA) and protein carbonyl (PC) were determined in testicular tissues and serum of rats. Testicular tissues were also examined histopathologically and Johnsen scores were determined. Results: Activities of SOD and GSH-Px in serum and testicular tissues were increased by I/R, but administration of CVD decreased these levels (p < 0.001 and p = 0.001). Significantly increased MDA levels in serum and testicular tissues were decreased by CVD treatment (p < 0.001 and p = 0.001). Concerning PC levels in serum and testicular tissues, there was no statistically significant difference between the groups (p = 0.989 and p = 0.428). There was not a statistically significant difference in terms of mean Johnsen scores between the groups (p = 0.161). Conclusions: Administration of CVD decreased oxidative damage biochemically in the rat testis caused by I/R injury, but histopathologically no change was observed between all of the groups. .

Lipid peroxidation and antioxidant status in lichen planus.

BACKGROUND: Lichen planus (LP) is an inflammatory skin disease of unknown aetiology. Recently, increased oxidative stress has been implicated in the pathogenesis of various skin diseases such as atopic dermatitis, psoriasis vulgaris and vitiligo. AIM: To evaluate the status of the oxidative stress and antioxidant defence system in patients with LP. METHODS: In total, 40 patients with LP (23 men, 17 women; mean +/- SD age 43.27 +/- 1.96 years) and 40 control subjects, matched for age and gender, were enrolled in this prospective study. The exclusion criteria included medication with immunosuppressive agents, history of trauma and surgery, and history of alcohol ingestion for at least 1 month prior to the study. The serum nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels and the erythrocyte catalase (CAT) levels were investigated in both groups. RESULTS: Mean +/- SD levels of serum NO (74.60 +/- 17.96 micromol/L) and MDA (18.24 +/- 5.21 micromol/L) in patients with LP were higher than those of the control group (P = 0.007 and P = 0.031, respectively). Serum SOD levels (18.19 +/- 3.71 U/mL) in patients with LP were also higher than in healthy controls (P = 0.002). In contrast, erythrocyte CAT levels (13 557.80 +/- 4134.42 U/kg haemoglobin) were significantly lower in the patient group than in the control group (P = 0.009). CONCLUSIONS: The findings of this study suggest that increased oxidative stress, increased lipid peroxidation and an imbalance in the antioxidant defence system may be involved in the pathogenesis of LP.

Caffeic acid phenethyl ester changes the indices of oxidative stress in serum of rats with renal ischaemia-reperfusion injury.

Oxygen-derived free radicals have been implicated in the pathogenesis of renal injury after ischaemia-reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. To investigate whether treatment with either CAPE or alpha-tocopherol modifies the levels of the endogenous indices of oxidant stress, we examined their effects on an in vivo model of renal ischaemia-reperfusion injury in rats. CAPE at 10 micromol kg(-1) or alpha-tocopherol at 10 mg kg(-1) was administered intraperitoneally before reperfusion. Acute administration of both CAPE and alpha-tocopherol altered the indices of oxidative stress differently in renal ischaemia-reperfusion injury.

50 endobronchial tuberculosis cases based on bronchoscopic diagnosis.

Endobronchial tuberculosis (ETB) is most often a complication of primary pulmonary tuberculosis in children, although it may also occur in adults. Bronchoscopically, mass lesion (polypoid and ulcerous granuloma), submucosal infiltration and fibrostenosis may usually be seen. 50 ETB cases were diagnosed by bronchial biopsy, bronchial fine needle aspiration and washing. Bronchoscopically, mass lesions were found in 31 cases (62%), 21 (42%) of which were ulcerous granulomas and 10 (20%) polypoid mass, while 11 (22%) cases were of submucosal infiltrative appearance, 16 (32%) fibrostenosis and 5 (10%) hyperaemia and oedema. The diagnosis could be made in 42 cases with bronchial biopsy, whereas only in 8 cases with bronchial fine needle aspiration. Statistically, therefore, the bronchial biopsy was found to be significantly more advantageous as compared to the other diagnostic methods for the diagnosis of ETB (p < 0.0001).

Evidence that the activities of erythrocyte free radical scavenging enzymes and the products of lipid peroxidation are increased in different forms of schizophrenia.

In order to examine antioxidant status and lipid peroxidation in schizophrenia patients, activities of three free radical scavenging enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)), and the level of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation have been studied in red blood cells. Schizophrenic patients were divided into three groups (disorganized (n = 21), paranoid (n = 26) and residual types (n = 18)) to determine differences between subgroups. SOD, CAT and GSH-Px activities in the control group were found to be 1461.0 +/- 248.6 U g(-1) Hb, 148.2 +/- 59.3 k g(-1) Hb and 25.87 +/- 4.25 U g(-1) Hb, respectively. We found no significant differences in SOD activities between study and control groups. There was a significant increase in SOD activity in the residual group compared to the paranoid group (P < 0.005). CAT activity was found to be increased in disorganized (148%), paranoid (147%), and residual (165%) groups compared to the control group. GSH-Px activity was markedly increased in the study groups except the paranoid group. Statistically significant (3-4 fold) increases in TBARS levels of red blood cells were found in all the study groups. It is proposed that antioxidant status may be changed in schizophrenia and thus may induce lipid peroxidation. Therefore, oxidative stress may have a pathophysiological role in all the subtypes of schizophrenia.