The effect of CPAP therapy on insulin-like growth factor and cognitive functions in obstructive sleep apnea patients.

OBJECTIVES: Cognitive impairment is common among patients with obstructive sleep apnea syndrome (OSAS). In this study, we aimed to investigate the effect of continuous positive airway pressure (CPAP) therapy on serum insulin-like growth factor-1 (IGF-1) levels and cognitive functions in patients with OSAS. PATIENT/METHODS: Thirty-three patients with newly diagnosed OSAS and 17 healthy-control subjects enrolled in the study. All individuals completed the mini-mental state examination (MMSE) to evaluate cognitive function. Blood samples were taken at the end of the polysomnography in the morning and the same procedures were repeated 3 months after starting CPAP treatment. RESULTS: In the OSAS group, the baseline MMSE score was 23.5 ± 3.6, and serum IGF-1 level was 79.1 ± 36.1 ng/mL. Both values were significantly lower compared with the control group (mean MMSE score = 28.1 ± 1.4, P = 0.0001; mean serum IGF-1 level = 147.1 ± 49.1 ng/mL, P < 0.0001). Three months after CPAP treatment, OSAS patients showed a significant improvement in MMSE scores (26.5 ± 2.8, P = 0.0001) and serum IGF-1 level (129.1 ± 58.2, P = 0.0001). In contrast, baseline and third-month measurements for IGF-1 levels and MMSE scores were not significantly different in the control group. CONCLUSIONS: The results indicate that effective CPAP therapy in OSAS patients leads to significant improvement in cognitive functions and IGF-1 even in a short-term follow-up. Cognitive function assessment might be a part of evaluation in OSAS patients.

The Association of Brain-Derived Neurotrophic Factor Gene Polymorphism with Obstructive Sleep Apnea Syndrome and Obesity.

BACKGROUND: Obesity represents a major risk factor for Obstructive Sleep Apnea Syndrome (OSAS). Brain-derived neurotrophic factor (BDNF) affects the mechanisms that regulate weight, eating behavior, and metabolism. This project aims to investigate the possible association of BDNF gene polymorphism with obesity and OSAS, and to contribute knowledge to the understanding of the pathophysiology of OSAS. METHODS: The subjects included in this study were selected among the individuals who were hospitalized in the Erciyes University Medical School Chest Diseases Sleep Medicine Laboratory. Subjects were divided into four groups based on the presence of OSAS and/or obesity. Group 1 included OSAS+ obesity+ patients, Group 2 included OSAS+ obesity- patients, Group 3 included OSAS- obesity+ patients, and Group 4 included OSAS- obesity- patients. The targeted patient number per each study group was 45, but only 32 patients could be enrolled into Group 3. RESULTS: Out of a total number of 167 subjects, 117 (70.1 %) had BDNF 196G/G, 48 (28.7 %) had BDNF 196G/A, and 2 (1.2 %) had BDNF 196A/A genotype. Of 48 subjects having BDNF 196G/A genotype, 32 (66.6 %) were obese, and 16 (33.3 %) were non-obese. Out of 90 subjects with OSAS, 64 (71.1 %) had BDNF 196G/G, and 25 (27.8 %) had BDNF 196G/A genotype. Out of 77 subjects without OSAS, BDNF 196G/G, and BDNF 196G/A genotypes were detected in 53 (68.8 %) and 23 (29.9 %) subjects, respectively. A statistically significant difference was demonstrated between the four study groups in terms of BDNF rs6265 polymorphism (p = 0.013). This difference was attributed to OSAS+ obesity- Group, in which BDNF 196G/G genotype was more common and BDNF 196G/A polymorphism was less common than the patients in other groups. CONCLUSION: In conclusion, BDNF 196G/A genotype was found to be more frequent among obese patients compared to the non-obese individuals, but it was not significantly related to OSAS in the present study. BDNF196G/G genotype was more common and BDNF 196G/A polymorphism was less common among OSAS+ obesity- subjects compared to the other study groups.

Altered expression of human endogenous retroviruses syncytin-1, syncytin-2 and their receptors in human normal and gestational diabetic placenta.

INTRODUCTION: Syncytins belong to the Human Endogenous Retrovirus family. The syncytin-1 receptor, SLC1A5, and syncytin-2 receptor, MFSD2, interact with their respective syncytin proteins to induce syncytiotrophoblast formation. However, there is no information about syncytins in gestational diabetic placenta. Therefore, we studied the expression and localization of syncytins and their receptors during normal placental development and in gestational diabetic placenta. METHODS: Immunohistochemistry and Western-blot methods were performed with antibodies against syncytin-1, syncytin-2, SLC1A5 and MFSD2 in human first trimester placental tissues, normal term and gestational diabetic placentas. Syncytin-1, syncytin-2 and MFSD2 mRNA transcripts were determined by qRT-PCR in normal and diabetic term placentas. RESULTS: Cytoplasmic syncytin-1, syncytin-2, SLC1A5 and MFSD2 immunoreactions were observed in the trophoblastic layers in all placental samples. Some of the stromal cells showed strong cytoplasmic punctate staining. There were significantly weak syncytin-2 and MFSD2 immunoreaction intensities in diabetic placentas by ImageJ analysis, in parallel with decreased syncytin-2 and MFSD2 proteins in diabetic placentas by Western-blot. Protein expression of SLC1A5 increased dramatically in early pregnancy compared to term placenta. Syncytin-1, syncytin-2 and MFSD2 mRNA transcripts showed similar relative expression pattern by qRT-PCR. DISCUSSION: Syncytins were localized not only in cytotrophoblast cells and the basement membrane of the syncytiotrophoblast but also in the apical microvillous membrane and cytoplasm of syncytiotrophoblast, and some of the stromal cells and endothelium. Decreased syncytin-2 and MFSD2 proteins in gestational diabetic placentas might cause abnormal syncytiotrophoblast formation and possibly be involved in the pathology. Therefore, our study highlights an important potential relationship between syncytins and gestational diabetic placenta.

Increased Expression of Matrix Metalloproteinase-9 in Patients with Temporal Lobe Epilepsy.

AIM: The molecular mechanism of epileptogenesis in temporal lobe epilepsy is still unclear. Experimental studies have suggested that matrix metalloproteinases have important roles in this process, but human studies are limited. The aim of this study was to assess the expression of MMP-9, MMP-2 and their tissue inhibitors (TIMP-1 and TIMP-2) in patients with temporal lobe epilepsy with hippocampal sclerosis (TLE-HS). MATERIAL AND METHODS: The tissue samples from temporal neocortex and hippocampus were obtained from patients with temporal lobe epilepsy with hippocampal sclerosis who had undergone anterior temporal lobectomy for recurrent medically resistant seizures. Immunohistochemical methods were used to determine the expression of MMP-9, MMP-2 and their tissue inhibitors. Tissue samples were also analyzed with transmission electron microscopy. RESULTS: The immunoreactivity for MMP-9 both in hippocampal and temporal neocortical neurons was stronger than that of MMP-2. Additionally, there was a mild reaction for its tissue inhibitor TIMP-1 as with TIMP-2. The TEM analysis of the hippocampus revealed that there was apparent ultra-structural damage on the pericarya and neuropil of some neurons. There was obvious damage in the mitochondria and the nuclear membrane. CONCLUSION: The preliminary results of this study revealed that MMP-9 may have a role in patients with drug resistant TLE-HS.

Correlation between pentraxin-3 and endothelial dysfunction in obstructive sleep apnea syndrome.

BACKGROUND AND AIM: Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for cardiovascular disease. Recent studies showed endothelial dysfunction and pentraxin-3 both of an early marker for development of cardiovascular disease. The aim of the study was to evaluate the relationship between severity of OSAS and endothelial dysfunction and inflammatory markers including pentraxin-3 and high-sensitivity C-reactive protein (hs-CRP). METHODS: This was a cross-sectional study in which patients who had undergone a polysomnographic study for diagnosis of OSAS were recruited. Included patients were grouped according to apnea-hypopnea index (AHI) as mild (AHI between 5 and 14.9) and moderate-severe OSAS (AHI ⩾ 15). Patients with AHI < 5 served as control group. Endothelial function was evaluated by flow-mediated dilatation (FMD). Serum pentraxin-3 and hs-CRP levels were measured. RESULTS: Eighty-three patients enrolled for the study. We found a significant increment in pentraxin-3 and hs-CRP levels and a significant decrement in FMD as the severity of OSAS increased. There was a negative correlation between FMD and AHI, pentraxin, and hs-CRP. CONCLUSION: OSAS patients have significantly elevated pentraxin-3 levels and endothelial dysfunction. Furthermore, both pentraxin-3 and endothelial dysfunction were independently associated with severity of OSAS defined by AHI.

Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor ß Pathway.

CTCFL, a paralog of CTCF, also known as BORIS (brother of regulator of imprinted sites), is a testis-expressed gene whose function is largely unknown. Its product is a cancer testis antigen (CTA), and it is often expressed in tumor cells and also seen in two benign human vascular malformations, juvenile angiofibromas and infantile hemangiomas. To understand the function of Ctcfl, we created tetracycline-inducible Ctcfl transgenic mice. We show that Ctcfl expression during embryogenesis results in growth retardation, eye malformations, multiorgan pathologies, vascular defects, and neonatal death. This phenotype resembles prior mouse models that perturb the transforming growth factor ß (TGFB) pathway. Embryonic stem (ES) cells with the Ctcfl transgene reproduce the phenotype in ES cell-tetraploid chimeras. Transcriptome sequencing of the Ctcfl ES cells revealed 14 genes deregulated by Ctcfl expression. Bioinformatic analysis revealed the TGFB pathway as most affected by embryonic Ctcfl expression. Understanding the consequence of Ctcfl expression in nontesticular cells and elucidating downstream targets of Ctcfl could explain the role of its product as a CTA and its involvement in two, if not more, human vascular malformations.

The role of Wnt signaling members in the uterus and embryo during pre-implantation and implantation.

Wnt family members are best known for their roles in cell fate determination, differentiation, proliferation and apoptosis during embryonic development. Wnt signaling becomes effective during these cellular processes through the proper interaction between its ligands, receptors, effectors and inhibitors. Here we review Wnt signaling in terms of embryonic development to the blastocyst stage implantation with emphasis on endometrial changes that are critical for receptivity in the uterus. The relationship between Wnt signaling and implantation clearly reveals that, Wnt family members are critical for both early embryonic development and changing of the endometrium before implantation. Specific Wnt signaling pathway members are demonstrated to be critical for endometrial events such as decidualization and endometrial gland formation in addition to cyclic changes in the endometrium controlled by reproductive hormones. In conclusion, specific roles of Wnt members and associated factors for both uterine function and embryonic development should be further investigated with respect to the efficiency of human ARTs.

Is Serum Cystatin C a Predictor of Acute Pulmonary Thromboembolism in Patients With Normal Renal Function?

Early diagnosis is the key point in the management of acute pulmonary thromboembolism (PTE). There are no reports in the literature comparing the serum cystatin C levels in patients with acute PTE and normal volunteers. Therefore, in this study, we analyzed 50 patients with acute PTE and 45 healthy volunteers with normal renal function. The serum cystatin C level was significantly higher in the PTE group than in the non-PTE group (1.08 mg/dL [interquantile range (IQR) 0.79-1.56] and 0.85 mg/dL [IQR 0.77-1.03], respectively, P = .017). When determining the presence of PTE, the highest value of sensitivity and specificity was set at a cutoff value of 1.15 mg/dL with 93.3% specificity, 46.0% sensitivity, 88.5% positive predictive value, and 60.9% negative predictive value. In the multivariate model, cystatin C was significantly associated with the presence of PTE (odds ratio: 12.34, 95% CI 2.64-57.75). In conclusion, cystatin C may be an indicator of acute PTE in patients with normal renal function.

Expression of vascular endothelial growth factor and transforming growth factor alpha in rat testis during chronic renal failure.

INTRODUCTION: Vascular endothelial growth factor (VEGF) is known to influence testis function. Transforming growth factor alpha (TGF-α) is expressed in the postnatal testis, and has been demonstrated to stimulate testis development. Systemic diseases such as chronic renal failure (CRF) interfere with hypothalamic-pituitary-gonadal axis, which may cause defective steroidogenesis and gonadal functions. The aim of this study was to investigate the expression and localization of VEGF and TGF-α in testicular tissues of experimental CRF model. MATERIAL AND METHODS: Experimental CRF was induced in rats by the resection of more than 85% of renal mass. The expression of VEGF and TGF-α in testicular tissues were assessed by immunohistochemistry on paraffin sections of control, CRF-nondialysed and CRF-dialysed rats. RESULTS: The microscopic evaluation of the testicular structure showed that CRF did not affect testicular histology. Immunohistochemical evaluation showed that VEGF was expressed in the cytoplasm of primary and secondary spermatocyte series as well as the early spermatids. Staining intensity was lower in spermatocytes going through the first meiotic division. TGF-α was expressed in the nuclei of spermatogonia and primary spermatocytes with stronger staining intensity in spermatogonia. The intensity of VEGF staining was similar in control and experimental animals, however, TGF-α expression was lower in the CRF group. CONCLUSIONS: The continuous expression of VEGF in spermatocytes and spermatids suggests that the applied model of CRF does not directly disrupt morphology of seminiferous epithelium, thus also spermiogenesis. However, difference between control rats and CRF group in TGF-α immunopositivity, which was localised in spermatogonial mitosis step, may suggest the interference of CRF with early stages of spermatogenesis.

Non-asbestos-related malignant pleural mesothelioma.

Malignant pleural mesothelioma (MPM) is an uncommon tumor derived from mesothelial lining cells. MPM has been described as an insidious neoplasm because of its long latency period. The tumor is typically found in patients several decades after asbestos exposure. We herein describe a 26-year-old patient with MPM who presented with pleural effusion. The patient had not been exposed to asbestos or erionite. There are few case reports of non-asbestos-related MPM in young patients. We report this case to remind physicians to consider MPM in the differential diagnosis of pleural effusion in young patients without exposure to asbestos or erionitis.

Is TNF-α gene polymorphism related to pulmonary functions and prognosis as determined by FEV1, BMI, COPD exacerbation and hospitalization in patients with smoking-related COPD in a Turkish population?

INTRODUCTION: Some conflicting results have been published about the relationship between TNF-α-308 gene polymorphism and chronic obstructive pulmonary disease (COPD). The aim of this study was to determine whether TNF-α-308 gene polymorphism was associated with smoking-related COPD and whether it was associated with pulmonary function parameters (PFTs), body mass index (BMI), and prognosis. METHODS: We studied the frequencies of TNF-α-308 gene polymorphism in 90 male subjects (60 subjects with COPD and 30 healthy smokers) in a Caucasian population. RESULTS: There was no significant difference in the frequency of G/G and G/A gene polymorphisms in the COPD group compared with control subjects (p>0.05). We compared COPD patients as G/A gene polymorphism and G/G gene polymorphism; the PFTs and BMI before and after one year were not statistically significant (p>0.05). Also, the exacerbation and hospitalization data of COPD patients were not significant between these groups. CONCLUSION: In conclusion, there was no difference between smoking-related COPD and the control group according to TNF α-308 gene polymorphism in a Caucasian population. In addition, it was shown that important determinants of prognosis of COPD such as FEV1, BMI, COPD exacerbation and hospitalization were not associated with TNF-α-308 gene polymorphism.

Learning curve of conventional transbronchial needle aspiration.

BACKGROUND AND AIMS: Intrathoracic lymphadenopathy usually occurs as a result of neoplasm, granulomatous diseases, infections or reactive hyperplasia. Conventional transbronchial needle aspiration (C-TBNA) is a cheap and safe procedure for diagnosing intrathoracic lymphadenopathy. The aim of this study was to assess the learning curve and diagnostic accuracy of C-TBNA after an observational education programme. METHODS: In the present study, we retrospectively evaluated our first 62 C-TBNA procedures at Erciyes University between May 2012 and December 2012 after an observational education programme. The first 31 patients were defined as group A, and the second 31 patients as group B. RESULTS: One hundred and seven lymph nodes were sampled in 62 patients by C-TBNA. Adequate lymph node samples were obtained in 52 of the 62 patients (83.8%). In these 52 patients, two patients had a diagnosis of 'suspicious of malignancy' by C-TBNA, and these patients were excluded from the analysis. In the remaining 50 cases who had adequate results, the sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and diagnostic accuracy per patient were 80.6%, 92.9%, 96.7%, 65.0% and 84.0%, respectively. The diagnostic accuracy rates of C-TBNA for Group A and B were 72.0% (18/25) and 96.0% (24/25), and the difference was statistically significant (P < 0.05). CONCLUSION: C-TBNA is a useful diagnostic procedure for sampling intrathoracic lymphadenopathies and masses that are adjacent to the bronchial system. An observational education programme is helpful for learning C-TBNA. The diagnostic yield improves in time, and approximately 30 procedures may be sufficient to achieve successful results.

Invasive pulmonary aspergillosis in patients with chronic obstructive pulmonary disease.

BACKGROUND: Invasive pulmonary aspergillosis (IPA) is an infection often occurring in neutropenic patients and has high mortality rates. In recent years, it has been reported that the incidence of IPA has also increased in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study is to investigate the clinical and demographic characteristics and treatment responses of IPA in patients with COPD. METHODS: Seventy-one patients with a positive culture of Aspergillus from lower respiratory tract samples were examined retrospectively. Eleven (15.4%) of these patients, affected with grade 3 or 4 COPD, had IPA. RESULTS: Aspergillus hyphae were detected in lung biopsy in three (27.3%) out of 11 patients and defined as proven IPA; a pathological sample was not taken in the other eight (72.7%) patients, and these were defined as probable IPA. Aspergillus isolates were identified as six cases of Aspergillusfumigatus and three of Aspergillusniger in nine patients, while two isolates were not identified at species level. While five patients required intensive care unit admission, four of them received mechanical ventilation. The most common finding on chest X-ray and computed tomography (CT) (respectively 63.6%, 72.7%) was infiltration. Amphotericin B was the initial drug of choice in all patients and five patients were discharged with oral voriconazole after amphotericin B therapy. Six patients (54.5%) died before treatment was completed. CONCLUSIONS: IPA should be taken into account in the differential diagnosis particularly in patients with severe and very severe COPD presenting with dyspnea exacerbation, poor clinical status, and a new pulmonary infiltrate under treatment with broad-spectrum antibiotics and steroids.

Mean platelet volume in patients with obstructive sleep apnea syndrome and its relationship with cardiovascular diseases.

Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for the development of cardiovascular events and hypertension. Mean platelet volume (MPV), an indicator of platelet activation and aggregation, is closely related with cardiovascular diseases (CVDs). We aimed to show the relationship between OSAS and MPV with CVD. The medical records of 205 patients who were admitted to the sleep study were evaluated. OSAS was diagnosed by polysomnography if the apnea-hypopnea index (AHI) was greater than 5. MPV was calculated from blood samples. According to AHI, individuals in whom AHI was less than 5 were recruited as the control group, those in whom AHI was 5-15 as the mild OSAS group, those in whom AHI was equal to 15-30 as the moderate OSAS group, and those in whom AHI was greater than 30 as the severe OSAS group. Of the patients, 137 (67%) were men and 68 (33%) were women; the mean age was 53.0±14.1 years. There were 35 (17%), 20 (10.2%), 42 (20.4%), and 108 (52.6%) participants in groups 1, 2, 3, and 4, respectively. There were significant differences in terms of coronary artery disease and hypertension between all groups (P<0.05). There was a significant association between the severity of OSAS and MPV in groups 3 and 4, whereas there was not any association in groups 1 and 2 (group 1=9.3±0.7, group 2=9.4±0.8, group 3=9.5±1.1, group 4=10.2±1.2; P for trend 0.03). We showed that MPV was significantly increased in patients with OSAS, which is an independent risk factor for CVD. Therefore, MPV could be used as a marker to predict CVD in OSAS.

A Rare Cause of Diffuse Parenchymal Lung Disease together with Granulomatous Reaction: Pulmonary Amyloidosis.

Amyloidosis is a heterogeneous group of disorder associated with the deposition of protein in an abnormal fibrillar form. Primary Sjögren's syndrome (PSS) is a systemic inflammatory disorder that commonly affects the exocrine glands. The reported frequency of pulmonary involvement in PSS varies widely, ranging from 9% to 75%. Pulmonary involvement occurs in light-chain (AL) amyloidosis and is uncommon in the reactive (AA) and hereditary forms. Herein we present a case of PSS associated diffuse multinodular amyloidosis in the lung. We followed up the patient without treatment for three years. There are only minimal lung symptoms related to lung infiltration. In conclusion, pulmonary involvement in SS is an extremely rare clinical manifestation and usually has a good survival rate without treatment.

Biphasic anaphylaxis to gemifloxacin.

Anaphylaxis have been documented as adverse effects of ciprofloxacin, ofloxacin, norfloxacin, levofloxacin, and moxifloxacin. However resistant and biphasic anaphlylactic reactions to gemifloxacin have not been reported to date. Management of severe anaphylaxis in the elderly can be complicated by concurrent medications such as beta (ß) adrenergic, alpha (α) adrenergic blockers and angiotensin-converting enzyme (ACE) inhibitors. We report here in the case of a 60-year-old male who was taking on ACE inhibitor, α and ß blockers and experienced a severe, resistant and biphasic anaphlylactic reaction to gemifloxacin mesylate.

Angiogenesis in neurological disorders: a review.

Angiogenesis, recruitment of new blood vessels, is an essential component of the metastatic pathway. These vessels provide the principal route by which tumor cells exit the primary tumor site and enter the circulation. For many tumors, the vascular density can provide a prognostic indicator of metastatic potential, with the highly vascular primary tumors having a higher incidence of metastasis than poorly vascular tumors. The discovery and characterization of tumor-derived angiogenesis modulators greatly contributed to our understanding of how tumors regulate angiogenesis. However, although angiogenesis appears to be a rate-limiting event in tumor growth and metastatic dissemination, a direct connection between the induction of angiogenesis and the progression to tumor malignancy is less well understood. In this review, we discuss the observations concerning the modulation of angiogenesis and their implications in various neurological disorders, as well as their potential impact on cancer therapy.

Triamcinolone up-regulates GLUT 1 and GLUT 3 expression in cultured human placental endothelial cells.

The placenta is a glucocorticoid target organ, and glucocorticoids (GCs) are essential for the development and maturation of fetal organs. They are widely used for treatment of a variety of diseases during pregnancy. In various tissues, GCs have regulated by glucose transport systems; however, their effects on glucose transporters in the human placental endothelial cells (HPECs) are unknown. In the present study, HPECs were cultured 24 h in the presence or absence of 0.5, 5 and 50 µmol · l(-1) of synthetic GC triamcinolone (TA). The glucose carrier proteins GLUT 1, GLUT 3 and GC receptor (GR) were detected in the HPECs. We showed increased expression of GLUT 1 and GLUT 3 proteins and messenger RNA (mRNA) levels (p < 0.05) after 24-h cell culture in the presence of 0.5, 5 and 50 µmol · l(-1) of TA. In contrast, GR protein and mRNA expressions were down-regulated (p < 0.05) with 0.5, 5 and 50 µmol · l(-1) of TA 24-h cell culture. The results demonstrate that GCs are potent regulators of placental GLUT 1 and GLUT 3 expression through GR. Excessive exposure to GCs causes maternal and fetal hypoglycemia and diminished fetal growth. We speculate that to compensate for fetal hypoglycemia and diminished fetal growth, the expression of placental endothelial glucose transporters might be increased.

Obstructive sleep apnea syndrome is related to the progression of chronic kidney disease.

BACKGROUND AND AIM: Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for the development of cardiovascular events and hypertension. The possible causes are oxygen desaturation due to hypopnea, increased cytokine levels and insulin resistance. All these risk factors also have a role in the progression of chronic kidney disease (CKD). The aim of this study was to determine the relationship between OSAS and the severity of CKD. MATERIALS AND METHODS: We retrospectively evaluated the medical records of 175 subjects who were admitted for the polysomnography study. OSAS was diagnosed by polysomnography if Apnea-Hypopnea Index (AHI) > 5 and glomerular filtration rate (GFR) was calculated with Cockcroft-Gault formula. According to AHI, individuals with AHI < 5 were recruited as group 1 (OSAS negative group), those with AHI = 5-15 group 2 (mild OSAS group), those with AHI = 15-30 group 3 (moderate OSAS group), and those with AHI > 30 group 4 (severe OSAS group). RESULTS: Of the subjects, 117 (67%) were men, 58 (33%) were women and the mean age was 54.0 ± 12.1 years. There were 28 (14.3%), 18 (10.3%), 35 (20.0%) and 97 (55.4%) patients in groups 1, 2, 3 and 4 respectively. The prevalence of diabetes mellitus and hypertension and body mass index was significantly higher in severe OSAS group (P < 0.05). A significant decrease in GFR was detected when the severity of OSAS increased (group 1 = 50.0 ± 11.8, group 2 = 44.8 ± 15.9, group 3 = 40.8 ± 14.7, group 4 = 38.8 ± 16.0; P for trend < 0.001). CONCLUSION: In the light of the present study, we speculate that OSAS is an independent risk factor for the progression of chronic kidney disease, which is a growing health problem. Further randomized-multicenter prospective studies are warranted to evaluate this relationship.

The prevalence of occupational asthma among denim bleachery workers in Kayseri.

The bleachery procedure is the most frequent method used to decolorize denims since sandblasting has been shown to cause silicosis. The aim of this study was to determined the prevalence of occupational asthma among denim bleachery workers in Kayseri. The study was conducted in 4 factories, in which jean bleachery was performed, in Kayseri between December 2008 and February 2009. Overall, forty-four subjects, 22 from the bleachery section and 22 from the other sections, were included. A questionnaire about respiratory symptoms was administered. Pulmonary function tests (PFTs) and serial peak expiratory flow (PEF) measurements were performed. All subjects were evaluated by posteroanterior chest x-rays. The prevalence of occupational asthma (OA) in the bleachery and other section workers was 23.8% and 9.1%, respectively (p> 0.05). Within workers, exercise dyspnea (23.3%) and wheezing (20.9%) were the most frequent symptoms. The relationship between the duration of employment and PFTs in bleachery workers (n= 21) was negatively correlated and statistically significant with FEV1, FEF25-75 (moderate; r= -0.477, -0.449, respectively; p< 0.05) and FEV1/FVC, FEV1% (well; r= -0.588, -0.509, respectively; p< 0.05). The results of the present study suggest that exposure to denim-bleaching agents plays an important role in the occurrence of respiratory symptoms, reduction in pulmonary functions, and induction of occupational asthma.