Protective effect of tadalafil on ischemia/reperfusion injury of rat ovary

Background/Purpose

The aim of the study was to evaluate the effects of tadalafil (TDF) on ischemia/reperfusion (I/R) injury in rat ovaries.

Methods

Thirty-five female Sprague-Dawley rats were randomly divided into 5 groups (n = 7): sham (S), I/R1, I/R2, TDF1, and TDF2. In the I/R1 and TDF1 groups, 3-hour ischemia was followed by 12-hour reperfusion; and in the I/R2 and TDF2 groups, 3-hour ischemia was followed by 24-hour reperfusion. In the TDF groups, 30 minutes before reperfusion, a single dose of 5 mg/kg TDF was administered intraperitoneally. The ovarian tissue levels of malondialdehyde and nitric oxide (NO), and the activities of superoxide dismutase and catalase were measured biochemically. Tissue damage to ovarian tissue was scored by histopathologic examination.

Results

The tissue malondialdehyde levels were significantly higher and the catalase and superoxide dismutase activities were significantly lower in the I/R groups compared with the S and TDF groups (P < .05). The NO levels were significantly higher in the TDF1 group than the S and I/R1 groups (P < .05). Although the NO levels were increased in the TDF2 group compared with the I/R2 group, the difference was not significant. Ovarian tissue damage scores of the I/R groups were significantly higher than those of the S group (P < .05). Treatment with TDF significantly decreased the ovarian tissue damage scores in the TDF groups compared with the I/R groups (P < .05).

Conclusions

Tadalafil is effective in preventing tissue damage induced by I/R in rat ovaries.     

Lack of correlation between Helicobacter pylori infection and autologous serum skin test in chronic idiopathic urticaria

BACKGROUND: There are controversial reports about the direct role of Helicobacterpylori infection in chronic idiopathic urticaria. The indirect role of H. pylori infection in the induction of pathogenetic antibodies is not fully elucidated either. This study aims to reveal the association of H. pylori infection with autologous serum skin test positivity in chronic idiopathic urticaria (CIU) patients. METHODS: A total of 47 patients (35 women, 12 men, age range 17-65 years) diagnosed as CIU were included in the study. Autologous serum skin test was performed on all patients. The patients were examined with a commercially available ELISA test for H. pylori-specific antibodies. Gastroscopy with mucosal biopsy and rapid urease tests were proposed to verify the presence of H. pylori infection. RESULTS: Helicobacter pylori infection was detected in 33 of the 47 patients (70%). No significant relation was found between the autologous serum skin test positivity and the serological and histopathological presence of H. pylori infection. CONCLUSION: The results of our study suggest that chronic H. pylori infection does not appear to have a role in the induction of autoantibodies in CIU.     

Pregnancy-related low back pain in women in Turkey: Prevalence and risk factors

Objectives

To investigate the prevalence of pregnancy-related low back pain (PRLBP) in women in Turkey, identify the factors associated with PRLBP and predict the risk of PRLBP.

The Akt inhibitor,triciribine, ameliorates chronic hypoxia-induced vascular pruning and TGFβ-induced pulmonary fibrosis

Background and Purpose

Interstitial lung disease accounts for a group of chronic and progressive disorders associated with severe pulmonary vascular remodelling, peripheral vascular rarefaction and fibrosis, thus limiting lung function. We have previously shown that Akt is necessary for myofibroblast differentiation, a critical event in organ fibrosis. However, the contributory role of the Akt-mTOR pathway in interstitial lung disease and the therapeutic benefits of targeting Akt and mTOR remain unclear.

Experimental Approach

We investigated the role of the Akt-mTOR pathway and its downstream molecular mechanisms in chronic hypoxia- and TGFβ-induced pulmonary vascular pruning and fibrosis in mice. We also determined the therapeutic benefits of the Akt inhibitor triciribine and the mTOR inhibitor rapamycin for the treatment of pulmonary fibrosis in mice.

Key Results

Akt1^−/− mice were protected from chronic hypoxia-induced peripheral vascular pruning. In contrast, hyperactivation of Akt1 induced focal fibrosis similar to TGFβ-induced fibrosis. Pharmacological inhibition of Akt, but not the Akt substrate mTOR, inhibited hypoxia- and TGFβ-induced pulmonary vascular rarefaction and fibrosis. Mechanistically, we found that Akt1 modulates pulmonary remodelling via regulation of thrombospondin1 (TSP1) expression. Hypoxic Akt1^−/− mice lungs expressed less TSP1. Moreover, TSP1^−/− mice were resistant to adMyrAkt1-induced pulmonary fibrosis.

Conclusions and Implications

Our study identified Akt1 as a novel target for the treatment of interstitial lung disease and provides preclinical data on the potential benefits of the Akt inhibitor triciribine for the treatment of interstitial lung disease.     

The spectrum of diseases causing fever of unknown origin in Turkey: a multicenter study.

OBJECTIVE: The purpose of this trial was to determine the spectrum of diseases with fever of unknown origin (FUO) in Turkey. METHODS: A prospective multicenter study of 154 patients with FUO in twelve Turkish tertiary-care hospitals was conducted. RESULTS: The mean age of the patients was 42+/-17 years (range 17-75). Fifty-three (34.4%) had infectious diseases (ID), 47 (30.5%) had non-infectious inflammatory diseases (NIID), 22 (14.3%) had malignant diseases (MD), and eight (5.2%) had miscellaneous diseases (Mi). In 24 (15.6%) of the cases, the reason for high fever could not be determined despite intensive efforts. The most common ID etiologies were tuberculosis (13.6%) and cytomegalovirus (CMV) infection (3.2%). Adult Still's disease was the most common NIID (13.6%) and hematological malignancy was the most common MD (7.8%). In patients with NIID, the mean duration of reaching a definite diagnosis (37+/-23 days) was significantly longer compared to the patients with ID (25+/-12 days) (p=0.007). In patients with MD, the mean duration of fever (51+/-35 days) was longer compared to patients with ID (37+/-38 days) (p=0.052). CONCLUSIONS: Although infection remains the most common cause of FUO, with the highest percentage for tuberculosis, non-infectious etiologies seem to have increased when compared with previous studies.     

Low scores on the Benton Facial Recognition Test associated with vertebrobasilar insufficiency

Background

Decreased posterior cerebral circulation has been observed in patients with vertebrobasilar insufficiency (VBI). Reduced cerebral perfusion may have an impact on mental performance as measured by the Benton Facial Recognition Test (BFRT). We evaluated the usefulness of BFRT in identifying cognitive decline in patients with VBI by correlating test performance with total blood flow in the vertebrobasilar system and other variables such as educational level and gender.

Materials and methods

Thirty-three participants without dementia (mini-mental state examination; MMSE >27) and cranial magnetic resonance imaging abnormality, but with atherosclerotic risk factors were involved in the study. Nineteen subjects had a total vertebrobasilar flow volume less than 200 ml/min (Group I), and 14 subjects had a flow volume more than 200 ml/min (Group II).

Results

The groups were similar in regard to gender, age, and educational level. BFRT results were 19.53 ± 3.12 and 22.36 ± 2.73 for Groups I and II, respectively (p = 0.01). The educational level was the main factor affecting the BFRT score in Group I (p = 0.04).

Discussion

BFRT is clearly impaired in VBI as measured by Doppler ultrasound examination. We concluded that the test appears to adequately distinguish cognitive levels between VBI and other patients. Additionally, our results suggest that education is associated with BFRT results, and for normative purposes, gender consideration is unnecessary. Further studies are needed to investigate the association between VBI and memory dysfunction in early dementia.     

Cytokine Expression Before and After Aspirin Desensitization Therapy in Aspirin-Exacerbated Respiratory Disease

Aspirin exacerbated respiratory disease (AERD) is induced by acetylsalicylic acid (ASA) and/or nonsteroidal antiinflammatory drugs (NSAIDs). Effects of desensitization on many mediators have been examined previously, but few studies addressed the influence of desensitization on T lymphocytes and T lymphocyte-derived cytokines. This study was performed to examine peripheral blood lymphocyte (PBL) cytokine expression in aspirin-sensitive patients who have asthma before and after aspirin desensitization. In this study, the release of interleukin-2 (IL-2), interleukin-4 (IL-4), and interferon-gamma (IFN-γ) by CD4+ T lymphocytes prior to aspirin desensitization were also measured at intracellular levels, and expression of these cytokines after 1 month aspirin desensitization was evaluated. Twelve patients with AERD were included in the study. Two different control groups were formed, one consisted of 15 healthy people and second 12 aspirin tolerant asthmatic (ATA) patients using aspirin. A blood sample was collected prior to desensitization, and the tests were repeated by taking a second blood sample 1 month after the 4-day desensitization treatment. The proportion of lymphocytes secreting IFN-γ in the study group was 15.61?±?4.40 % before desensitization and 15.08?±?5.89 % after desensitization. The rate of IFN-γ secreting CD4+ T lymphocytes was 20.51?±?4.41 % in the normal control group and 16.07?±?5.7 % in the ATA group (p?=?0.021). The ratio of CD4+ T lymphocyte secreting IFN-γ was reduced in patients with AERD before desensitization compared to normal control group (p?=?0.040). The levels of IL-2, IL-4, and the subsets of lymphocyte were not different before and after desensitization compared to control groups.