Chronic fatigue immune dysfunction syndrome (CFIDS) is a central nervous system dysfunction characterized by profound disabling fatigue of at least 6 months and accompanied by multisystemic involvement manifesting itself with neuropsychiatric, neuroendocrinologic and immunologic symptoms. This review summarizes the current knowledge about CFIDS, which is little known in Turkish medical literature. Case definition, clinical presentation, evaluation, treatment and pathogenetic theories of CFIDS will be discussed in the light of the relevant literature. CFIDS is diagnosed on the basis of the clinically defined criteria. Patients with CFIDS experience profound functional impairment resulting in a significant decrease in their quality of life. Several research findings suggest that CFIDS is one of the stress-mediated disorders and should be distinct from psychiatric disorders. Existing pathophysiological abnormalities suggest that CFIDS is a heterogeneous condition of complex multifactorial etiology. Accumulating evidence also considers that dysfunction of HPA axis and serotonergic pathways in central nervous system may play an important role in the pathogenesis of CFIDS. Treatment for CFIDS is not specific but symptom-based and aimed at decreasing the level of stress. Graded exercise and cognitive behavioral therapy may be effective in increasing fitness and learning to cope with this disabling catastrophic syndrome, respectively. It has been reported that some experimental agents may be beneficial for treatment of some CFIDS patients. CFIDS is unlikely to be caused by a single agent. The data indicate that many environmental or psychological factors may precipitate or perpetuate the illness in genetically vulnerable subjects. The assessment and management of CFIDS patient should be multidimensional and psychiatrist should be a pervasive member of the multidisciplinary team for CFIDS. Kronik Yorgunluk İmmün Disfonksiyon Sendromu Nedir ? Kronik yorgunluk immün disfonksiyon sendromu (CFIDS) nöropsikiyatrik, nöroendokrinolojik, immünolojik semptomlarla kendini gösteren multisistemik tutulumlu, 6 aydan fazla süreli sakatlayıcı ve ağır bitkinlik ile karakterize bir santral sinir sistemi işlev bozukluğudur. Bu gözden geçirme yazısı Türkçe tıbbi literatürde pek az yer alan CFIDS hakkı ndaki güncel bilgileri özetlemektedir. CFIDS’in klinik tanımlaması, değerlendirmesi, tedavisi ve patogenetik teorileri ilgili literatürün ışığında tartışılacaktır. CFIDS klinik kriterlere dayalı olarak teşhis edilir. CFIDS hastaları hayat kalitelerinde önemli bir azalma ile sonuçlanan ağır bir işlevsel bozulma yaşarlar. Birçok çalışmanın bulgularına dayanılarak, CFIDS’in stresin aracılık ettiği bozukluklar sınıfına dahil bir sendrom olduğu ve psikiyatrik bozukluklardan ayırılması gerektiği ileri sürülmektedir. Mevcut patofizyolojik anormallikler CFIDS’in kompleks ve multifaktoriyel etyolojili heterojen bir durum olduğunu düşündürmektedir. Biriken deliller de santral sinir sisteminde HPA eksenin ve serotonin yolaklarının işlev bozukluğunun CFIDS patogenezinde önemli rol oynayabileceğini akla getirmektedir. CFIDS tedavisi özgün olmayıp semptomlara ve stres düzeyini düşürmeye yöneliktir. Tedricen artırılan egzersizin fiziksel kondisyonu iyileştirmede, bilişsel davranışçı tedavinin ise bu sakatlayı cı katastrofik sendromla başa çıkmayı öğrenmede etkili olabileceği düşünülmektedir. Deneysel tedavilerin bazı CFIDS hastaları için faydalı olabileceği de bildirilmektedir. CFIDS tek bir sebebe bağlı gibi görünmemektedir. Veriler genetik bakı mdan yatkınlığı olan şahıslarda birçok çevresel ve psikolojik faktörün sendromu başlatabileceğini veya şiddetlendirebileceğini göstermektedir. CFIDS hastasının değerlendirilmesi yanında tedavisi de çok boyutlu olarak yapılmalıdır ve psikiyatrist CFIDS multidisipliner ekibinin daimi bir üyesi olmalıdır.

Objective: The exact mechanism of the action of electroconvulsive therapy (ECT) has yet to be established. In this study, we aimed to test the hypotheses that ECT may cause acute alterations in pituitary hormones and that these hormonal responses to ECT may change throughout repeated ECT sessions. Methods: Nineteen depressed inpatients (8 males, 11 females; mean age ± SD= 44.77 ± 10.59 years) were undergone to 7 ECT sessions under general anaesthesia using propofol (1mg/kg). During the first and seventh ECTs, blood samples were collected 1 min before (baseline) and 2 min after propofol, immediately after ECT, and 30 and 60 min after ECT for measurements of serum prolactin (PRL), adrenocorticotropin (ACTH), cortisol, growth hormone (GH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH). Results: The results of the study confirmed that ECT had highly selective stimulatory effects on the release of PRL, ACTH and cortisol, but not on GH, FSH and LH. The hormonal responses to ECT did not change throughout ongoing ECT procedures, and did not differ between males and females. Conclusions: Whether there is a causal relationship between these neuroendocrine responses and the therapeutic effect of ECT is remain uncertain.

Both basic and clinical studies have shown that lithium can affect the pituitary-adrenocortical axis. In this study, we sougl test the hypothesis that prophylactic lithium (Li) treatment can induce alterations in cortisol secretion in euthymic bipolar ] ents and the length of Li administration can affect the degree of alterations. 2İ euthymic bipolar patients (mean±SD 34.90±10.05) on long-term lithium carbonate treatment for more than 6 months and 15 euthymic bipolar patients (mean±SD 29.53±8.76) on short-term Li therapy for shorter than 6 months who met DSM-IV criteria for bipolar affective disorder were luded in the study. 17 healthy control subjects (mean±SD age: 33.88±1.72) were chosen among the hospital staff. Serum t cortisol values were within the normal limits in all study groups but they were significantly lower in the Li-treated patients those of the controls. However, there was no difference between the two patient groups in plasma basal cortisol values, study documents that Li administration induces a significant reduction in cortisol release in bipolar patients compared tc normal control subjects, but cortisol secretion remains quite stable during the prolonged Li treatment. However, since basal tisol concentrations show considerable intraindividual and interindividual variations further studies are needed. Bipolar affektif hastalarda kısa ve uzun süreli lityum tedavisinin serum kortizol seviyelerine etkisi Temel ve klinik çalışmalar lityumun pitüiter-adrenal kortikal ekseni etkileyebildiğini göstermiştir. Biz bu çalışmada profili lityum tedavisinin ötimik bipolar hastalarda kortizol sekresyonunda değişiklik oluşturabileceği ve lityum tedavi süresini değişiklikleri etkileyebileceği hipotezini araştırdık. Çalışmaya DSM-IV teşhis kriterlerini karşılayan ve 6 aydan uzun süre yum tedavisi altında olan 20 ötimik bipolar hasta (ort±SD yaş: 34.90+10.05) ile 6 aydan kısa süredir lityum tedavisi altında 15 ötimik bipolar hasta (ort.±SD yaş: 29.53+8.76) dahil edildi. 17 sağlıklı kontrol şahıs (ort.±SD yaş: 33.88±1.72) hastahane söneli arasından seçildi. Serum bazal kortizol değerleri bütün çalşma gruplarında normal sınırlar içinde olmakla beraber, lit ile tedavi edilen hastalarda kontrollerinkinden önemli şekilde düşük bulundu. Bununla beraber, iki hasta grubu arasınd rum kortizol değerleri bakımdan önemli fark mevcut değildi. Bizim çalışmamız lityumun bipolar hastalarda kortizol salını normal kontrol şahıslardakine nazaran önemli şekilde azalttığını ortaya koymaktadır, fakat kortizol sekresyonu uzun süre yum tedavisi esnasında oldukça sabit bir şekilde kalabilmektedir. Yine de, bazal kortizol seviyeleri aynı şahısda ve şahı şahısa önemli değişiklikler gösterdiği için bulgularımızı teyid etmek üzere başka çalışmalara ihtiyaç vardır.

Objective: Although there are conflicting results, lithium carbonate has been demonstrated to induce the production of haematopoietic cells, particularly white blood cell series. In this study, we examined the effects of lithium on white blood cells in association with granulocyte colony-stimulating factor (G-CSF), which is a polypeptide growth factor that regulates the production of neutrophilic granulocytes. Methods: Eighteen lithiumnaive (8 females, 10 males; mean±SD age: 36±7.9 years) and 20 long-term lithium treated (9 females, 11 males; mean±SD age: 37.4±9.5 years) bipolar patients were included in the study. In the lithium-naive patients, lithium treatment was started to provide prophylactic serum lithium concentrations after blood samples were taken to determine the baseline haematological values (white blood cell, granulocyte and lymphocyte counts, haematocrit and G-CSF concentration). Blood samples were reobtained in the first and fourth weeks in this group. The same measurements were fulfilled once in the patients on the longterm lithium treatment. Results: The values of granulocyte count were significantly increased in the fourth week of lithium administration compared to the baseline values in the patients who were in the short-term lithium treatment, and this increase was associated with some elevation of G-CSF values that did not reach significance. The values of granulocyte count in the longterm lithium group were not significantly different from those of the baseline values of lithium-naive patients. Conclusion: Granulocytosis induced by lithium treatment in bipolar patients cannot be explained solely by the stimulation of G-CSF activity. Increased granulocyte count seems to approach the baseline values during the long-term lithium treatment. Bipolar affektif bozukluklu hastalarda lityum tedavisinin granulositler ve granülosit uyarıcı faktör üzerine etkisi Amaç: Tartışmalı sonuçlar olsa da, lityum karbonatın hematopoetik hücreler ve özellikle beyaz kan hücrelerinin üretimini artırdığı bildirilmiştir. Bu çalışmada lityumun beyaz küre hücreleri ve nötrofilik granülositlerin üretimini düzenleyen bir polipeptid büyüme faktörü olan granülosit koloni uyarıcı faktör (G-CSF) üzerine etkileri araştırıldı. Yöntem: Çalışmaya henüz hiç lityum kullanmamış 18 (8 kadın, 10 erkek; yaş ortalaması: 36±7.9) ve uzun süredir lityum kullanmakta olan 20 (9 kadın, 11 erkek; yaş ortalaması: 37.4±9.5) bipolar hasta alındı. İlk gruptaki hastalardan lityum başlanmadan önce ve başlandıktan sonraki 1. ve 4. haftalarda hematolojik değerleri (beyaz küre, granülosit ve lenfosit sayıları, hematokrit ve G-CSF değerleri) tespit etmek üzere üç kez kan alındı. Uzun süreli lityum grubunda aynı ölçümler bir kez yapıldı. Bulgular: Kısa süreli lityum grubunda lityum başlanmasının 4. haftasındaki granülosit sayısı bazal değerlere oranla anlamlı biçimde artmış bulundu, ve bu artış G-CSF değerlerinde anlamlılık düzeyine ulaşmayan bir miktar artışla birlikteydi. Uzun süreli lityum grubundaki granülosit sayısı ise henüz lityum başlanmamış hastaların bazal değerlerinden farklı bulunmadı. Sonuç: Bipolar hastalarda lityum tedavisinin yol açtığı granülositozis yalnızca G-CSF aktivitesinin uyarılmasıyla açıklanamaz. Lityum tedavisine bağlı olarak artan granülosit sayısı uzun süreli tedavi boyunca normale dönüyor gibi görünmektedir.

Objective: Lithium carbonate may affect calcium metabolism and alter parathyroid physiology. The purpose of this study was to test the hypothesis that long-term lithium treatment can induce alterations in serum total calcium and biologically active (intact) parathormone (PTH) levels in euthymic bipolar patients. Method: Serum total calcium levels were measured with standard autoanalyzer techniques, and intact PTH (iPTH) levels were assessed by RIA in 10 lithium-naive (mean age±SD: 34.50±4.85) and 15 long-term lithium treated (mean age±SD: 34.46±10.16) bipolar patients. -,143+Results: Both serum total calcium and iPTH levels were found significantly higher in the lithium treated group compared to lithium-naïve group and there was a positive correlation between these two biochemical variables. Conclusion: These data demonstrate that long-term lithium treatment may alter serum calcium and PTH activity. Bipolar bozukluğu olan hastalarda lityumun yol açtığı parathormon fonksiyon değişiklikleri Amaç: Lityum karbonat kalsiyum metabolizmasını ve paratiroid fizyolojisini etkileyebilir. Bu çalışmanın amacı ötimik bipolar hastalarda uzun süreli lityum tedavisinin serum total kalsiyum ve biyolojik olarak aktif (intakt) parathormon (PTH) düzeylerini değiştirebileceği hipotezini araştırmaktı. Yöntem: Bu amaça, 10 hiç lityum kullanmamış (yaş ortalaması SS: 34.50?4.85) ve 15 uzun süredir lityum kullanmakta olan (yaş ortalamas?SS: 34.46?10.16) bipolar hastanı serum total kalsiyum ve intakt parathormon (iPTH) düzeyleri sırasıyla standart otoanalizer ve RIA teknikleri ile ölçüldü. Bulgular: Uzun süreli lityum tedavisi almakta olan hastalarda lityum kullanmamış hastalara göre serum total kalsiyum ve iPTH değerlerinin her ikisinin de birbiriyle ilişkili olarak yüksek olduğu bulundu. Sonuç: Bu bulgular uzun süreli lityum tedavisinin, serum kalsiyum PTH fonksiyonların değiştirebileceğini ortaya koymaktadır.

Objective: Chronic fatigue immune dysfunction syndrome (CFIDS) is a debilitating disease characterized by physical and mental fatigue for at least 6 months. The etiology of CFIDS is heterogeneous. Hypothalamic-pituitary-adrenal (HPA) axis dysfunction is considered one of the underlying pathophysiological mechanisms. The results of the studies investigating HPA axis activity in CFIDS are quite conflicting. This study aimed to investigate HPA axis activity in patients with CFIDS and the effect of corticosteroid treatment on HPA axis activity. Method: Thirty-four patients with CFIDS who did not have any psychiatric co-morbidity and who were diagnosed according to Centers for Disease Control (CDC) criteria and 22 physically and mentally-healthy subjects were included in the study. The HPA axis activity was evaluated by basal serum cortisol and dehydroepiandrosterone sulfate (DHEAS) and cortisol and DHEAS responses to low-dose adrenocorticotrophic hormone (ACTH) test. The procedure was repeated after four-week dexamethasone treatment (1.25mg/day). 20 patients were able to complete the trial. The procedure was performed only once in the control subjects. Results: There were no significant differences in basal serum cortisol and DHEAS levels, peak hormone responses or area under the hormone response curve between the patients and the controls in pre-treatment. While cortisol response to ACTH was statistically significant in the patients and controls, DHEAS response was not. The hormone responses to ACTH did not differ between the patients and controls. In the patients, peak DHEAS value was significantly reduced after dexamethasone treatment compared to those in pre-treatment. Conclusion: The results of the study suggest that serum cortisol and DHEAS levels and cortisol and DHEAS responses to ACTH in patients with CFIDS did not differ from healthy controls. These results do not support the hypotheses that patients with CFIDS have HPA dysfunction. Nevertheless, further studies are needed to confirm the results.

OBJECTIVE:Mental fatigue, cognitive disorders, and sleep disturbances seen in chronic fatigue syndrome (CFS) may be attributed to cholinergic deficit. A functional deficiency of cholinergic neurotransmission may cause the hypothalamic-pituitary-adrenal axis hypoactivity seen in CFS. Therefore, we investigated the alterations in stress hormones such as cortisol and dehydroepiandrosterone sulfate (DHEAS) in CFS patients before and after 4-week administration of galantamine hydrobromide, a selective acetylcholinesterase inhibitor, and aimed to investigate whether there are any relationships between the probable hormonal changes and cholinergic treatment.METHODS:Basal levels of cortisol and DHEAS were measured in 29 untreated CFS patients who were diagnosed according to Centers for Disease Control (CDC) criteria and in 20 healthy controls. In the patient group, four weeks after 8 mg/d galantamine hydrobromide treatment, cortisol and DHEAS levels were measured again. After the treatment 22 patients who stayed in study were divided into two subgroups as responders and nonresponders according to the reduction in their Newcastle Research Group ME/CFS Score Card (NRG) scores.RESULTS:Important findings of this study are lower pre-and post-treatment cortisol levels and in all CFS patients compared to controls (F=4.129, p=0.049; F=4.803, p=0.035, respectively); higher basal DHEAS values and higher DHEAS/cortisol molar ratios which were normalized following four weeks' treatment with 8 mg/d galantamine hydrobromide in the treatment-respondent group (F=5.382, p=0.029; F=5.722, p=0.025, respectively).CONCLUSION:The findings of the decrease in basal DHEAS levels and DHEAS/cortisol molar ratios normalizing with galantamine treatment may give some support to the cholinergic deficit hypothesis in CFS.

Objective: Folic acid and vitamin B12 are essential cofactors in several biochemical pathways that are critical for neurobiological and hematological functions. Vitamin B12 and folate deficiencies are reported in schizophrenia and depression patients but there are only a few studies investigating the effects of the treatment on serum folic acid and vitamin B12 levels. This study aimed to investigate serum folic acid and vitamin B12 levels in patients with depression, schizophrenia and bipolar disorder and the effects of the drug treatment on these vitamin levels.Method: Twenty-six schizophrenia, 16 major depressive, and 47 bipolar (manic, depressive or mixed episode) disorder inpatients diagnosed according to DSM-IV criteria and 21 healthy controls were included in the study. Serum vitamin B12 and folic acid levels were measured before the treatment. The patients received the treatment at therapeutic doses for 5 weeks. Fifteen of the schizophrenic patients were treated with atypical antipsychotics including risperidone, olanzapine, quetiapine and 11 of them with typical antipsychotics (haloperidol or zuclopenthicsole). Bipolar patients received mood stabilizer and antipsychotic and/or antidepressant according to their present episode. The patients with major depressive disorder were treated with various antidepressant drugs. Serum vitamin B12 and folic acid levels were measured again in all patients after five weeks. The same measurements were performed only once in the controls.Results: Serum folic acid and vitamin B12 levels were not significantly different among the patient groups and the controls in pre-treatment. In schizophrenic patients, serum folic acid levels were significantly reduced after typical antipsychotic treatment compared to those in pretreatment and to those of the controls while they did not change after atypical antipsychotic treatment. Bipolar patients who received lithium had lower serum folic acid levels in post-treatment than in pre-treatment. There was a negative correlation between serum folic acid levels and severity of depression in the patients with major depressive disorder.Conclusion: The results of the study suggest that serum folic acid and vitamin B12 values in schizophrenia, bipolar disorder, and major depressive disorder did not differ from healthy controls. However, it seems that some drug treatments might lead to a decrease in folic acid levels. Nevertheless, further studies are needed to confirm the effects of specific drug treatments on these vitamins.

AIMS Thyroid dysfunction is a known finding in alcoholism. Most studies have reported the reduction in peripheral thyroid hormones in acute withdrawal and long-term abstinence periods of alcohol dependence. The aim of the present study was to investigate the alterations of free thyroid hormones in early and late withdrawal and their association with aggression, age of onset, and family history of alcoholism. METHODS Male inpatients (n = 39; mean age +/- SD: 42.55 +/- 8.02 years) in alcohol withdrawal were compared with healthy men (n = 28; mean age +/- SD: 38.31 +/- 9.26 years). Levels of free thyroxine (fT4), free triiodothyronine, (fT3) and thyrothrophin (TSH) were measured in early (first day) and late (28th day) withdrawal in the patients and only once in the controls. RESULTS In early withdrawal, levels of thyroid hormones did not differ from those in the controls. In late withdrawal, fT3 and fT4 levels (2.71 +/- 0.56 and 10.80 +/- 1.86 pg/ml) were lower than those of both controls (3.32 +/- 0.41 and 11.95 +/- 1.49 pg/ml, respectively, P < 0.05 in both cases) and patients in early withdrawal (3.18 +/- 0.72 and 12.68 +/- 2.50 pg/ml, respectively, P < 0.05 in both cases). Patients were divided into subgroups according to aggression level, onset age of alcoholism, and family history. While the high-aggression group had lower serum levels of fT3 and fT4 in late withdrawal (2.49 +/- 0.41 and 10.44 +/- 2.15 pg/ml) compared with those of controls (P < 0.05 in both cases), the low-aggression group only had lower serum levels of fT3 in late withdrawal (2.90 +/- 0.62 pg/ml) compared with those of controls (P < 0.05). fT3 and fT4 values in the family history-negative group (2.67 +/- 0.56 and 10.75 +/- 1.88 pg/ml) were lower than those of controls in late withdrawal (P < 0.05 in both cases). Both fT3 and fT4 levels in late withdrawal (2.69 +/- 0.54 and 10.83 +/- 1.96 pg/ml) were decreased in early-onset group compared with those of controls (P < 0.05 in both cases). CONCLUSION Decreased free thyroid hormone levels may be a result of heavy alcohol consumption or a trait marker of alcoholism, especially in high-aggressive, early-onset and family history-negative patients.

We investigated the acute and lasting effects of electroconvulsive therapy (ECT) on the thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) in patients with depression. The TRH stimulation test was conducted (1) under basal conditions, after a first ECT, and at the end of a therapeutic course of 7 ECTs in 20 inpatients with depression; (2) before the initiation of antidepressant therapy and after the therapeutic response in 16 other inpatients with depression who responded to antidepressant drug treatment; and (3) in 20 healthy control subjects. Baseline TSH levels were lower in patients with depression, especially in those with more severe depression who were considered appropriate for ECT. Before the treatment, TSH response to TRH did not differ between the patients with depression and controls; however, more blunted TSH responses to TRH were observed in these patients compared with the controls. TSH response to TRH changed neither with one ECT nor throughout consecutive ECT sessions in patients with depression. Drug treatment also was found to have no impact on this response. These findings suggest that the therapeutic action of ECT in depression is not directly related to its effects on the hypothalamic-pituitary-thyroid axis. However, possible delayed effects of ECT on the HPT axis function should not be overlooked.

Dopamine D(2) blocking typical antipsychotic drugs are known to change the cerebral perfusion patterns of schizophrenic patients, especially in the frontal cortex and basal ganglia. In recent years atypical antipsychotics such as olanzapine, which have high serotonin 5-HT(2A)/dopamine D(2) occupation ratios, have been shown to be more effective in the treatment of schizophrenia symptoms. The aim of this study was to evaluate the regional cerebral blood flow (rCBF) of the schizophrenic patients treated with olanzapine in a within-subject design. Twenty-four patients with schizophrenia participated as subjects in the study. Each subject was scanned in a medication-free state and after 6 weeks of 10 mg/day fixed dose olanzapine treatment. Despite the clinical improvement seen in the patients, repeated-measures analysis of variance showed that olanzapine produced no significant changes in cortical rCBF after the six-week treatment. This finding indicates that unlike typical antipsychotics olanzapine has no negative effect on cortical cerebral perfusion patterns of schizophrenic patients.

. We have not encountered any brain single-photon emission tomography (SPET) study performed in adolescent depressed patients in the literature. Therefore, we used technetium-99m hexamethylpropylene amine oxime ( 99m Tc-HMPAO) brain SPET in adolescent patients with major depressive disorder (MDD) to examine the possible changes in cerebral perfusion and the possible association between perfusion indices and clinical variables. Fourteen adolescent out-patients (nine females, five males; mean±SD age: 13.11±1.43 years; range: 11–15 years) fulfilling the DSM-IV criteria for MDD and 11 age-matched healthy control subjects (six females, five males; mean±SD age: 13.80±1.60 years; range: 12–15 years) were included in the study. 99 Tc-HMPAO brain SPET was performed twice in the patient group and once in the control group. The first SPET investigation was performed under non-medicated conditions and the second was performed after depressive symptoms had subsided. A relative perfusion index (PI) was calculated as the ratio of regional cortical activity to the whole brain activity. We found significant differences between the PI values of the untreated depressed patients and those of the controls, indicating relatively reduced perfusion in the left anterofrontal and left temporal cortical areas. No significant differences in regional PI values were found between the remitted depressed patients and the controls. Our study suggests that adolescent patients with MDD may have regional cerebral blood flow deficits in frontal regions and a greater anterofrontal right-left perfusion asymmetry compared with normal subjects. The fact that these abnormalities in perfusion indices have a trend toward normal values with symptomatic improvement suggests that they may be state-dependent markers for adolescent MDD.

In the present study, we describe a method that we developed to isolate total RNA from porcine adipose tissue. This method entails homogenizing porcine adipose tissue in 10 ml of 4 m guanidium thiocyanate, 25 mm sodium citrate, 0.5% Sarcosyl, 0.1 m β-mercaptoethanol, pH 7.0, and then performing two CHCl3 extractions to remove lipid before following the procedure described by P. Chomczynski and N. Sacchi (1987, Anal. Biochem. 162, 156–159). This modification improved the yield of RNA approximately threefold (yield was 88 ± 7 μg total RNA/g of tissue) without affecting RNA quality.

We analyzed the carbohydrate moiety of purified alpha-l-acid glycoprotein (AGP) from Lewis adult male rats that were healthy (AGPh) or had experimental polyarthritis (AGPi). Sodium dodecyl sulfate polyacrylamide gel electrophoresis before and after N-glycanase treatment showed that AGPi had a slightly lower molecular mass (43 kDa vs. 45 kDa for AGPh) due to a lesser carbohydrate content. Carbohydrate analysis of purified AGP showed a slight decrease in the sialyl and galactosyl molar ratio in polyarthritis. However, the same difference in AGPh and AGPi (i.e. 0.6 residue) between the sialyl and galactosyl molar ratio indicated more than one sialyl residue per complex-type branch. Affinity for concanavalin A (ConA) of the whole glycoprotein and released oligosaccharides showed a progression during polyarthritis towards more reactive glycoforms or more ConA-bound oligosaccharides. Anion-exchange HPLC of the ConA-fractionated oligosaccharides corroborated the decreased sialylation in polyarthritis. Taken together, these results suggest a fall in branched and sialylated oligosaccharides during experimental polyarthritis. These structural changes might be related to an increase in Galβ 1–4GlcNAc α2–6 sialyltransferase activity described elsewhere in inflammatory states.

SUMMARY: P300 ABNORMALITY DUE TO CHRONIC ALCOHOL EXPOSURE IN PATIENTS WITH ALCOHOL DEPENDENCE Objective: Scalp recorded P300, the long latency event-related potential (ERP) occurring in response to stimulus is primarily originated from subcortical structures, has been reported to be an indicator of neuronal structure change. In this study, we aimed to examine the probable effect of chronic exposure to alcohol on ERP components in patients with alcohol dependence who had not overt cognitive dysfunction. Method: Twenty-six male patients (mean±SD age: 45.04±5.98 range: 2652) with alcohol dependence diagnosed to DSM-IIIR criteria and 15 male healthy control (mean ± SD age: 43.2±6.96± range: 28-54) were included in the study. Cognitive functions were evaluated with Mini Mental State Examination and Bender Gestalt teats. No overt structural abnormality detected in brain computerized tomography. Auditory ERPs were recorded by odd ball two voice discrimination task procedure in the third week of alcohol withdrawal. Results: We found that the patients had significantly longer P3 latency. P3 amplitude was not different from those of the controls. Conclusions: We concluded that our finding of delay P3 latency may indicate a neuronal structure impairment due to alcohol in patients with alcohol dependence despite the fact that obvious cognitive dysfunction is not observed.