Quercetin protects embryonic chicken spermatogonial cells from oxidative damage intoxicated with 3-methyl-4-nitrophenol in primary culture

Diesel exhaust particles (DEP) are considered to be one of the most important air pollutants. In this study, the protective effect of quercetin, an antioxidant flavonoid, on oxidative damage of testicular cells was studied by analysis of the intracellular antioxidant system of embryonic chickens after treatment with 3-methyl-4-nitrophenol (PNMC) derived from DEP. Testicular cells from 18-day-old embryos were cultured in serum-free McCoys’5A medium and challenged with PNMC (10⁻⁷ to 10⁻⁵ M) alone or in combinations with quercetin (1.0 μg/ml) for 48 h. Results showed that exposure to PNMC (10⁻⁵ M) induced condensed nuclei and vacuolated cytoplasm, a decrease in testicular cell viability and spermatogonial cell number. Exposure to PNMC induced lipid peroxidation by an elevation of thiobarbituric acid reactive substances as well as decreasing glutathione peroxidation activity and superoxide dismutase activity. However, simultaneous supplementation with quercetin restored these parameters to the similar levels as the control. PNMC is therefore concluded to have induced the oxidative stress of the spermatogonial cells, which can be attenuated by combined quercetin treatment. Our results support the therapeutic use of quercetin in the prevention or treatment of the reproductive toxicity by environmental toxicant PNMC.     

Endoscopic examination for duodenal ulcer bleeding during transcatheter arterial embolization: analysis of two cases

Endoscopy is usually effective in treating duodenal ulcer bleeding, but depending on the lesion site and overall patient condition, hemostasis may be difficult to achieve with endoscopy alone. We described two patients with duodenal ulcer bleeding in whom endoscopic hemostasis was difficult. Immediately after transcatheter arterial embolization, endoscopic examination was used to confirm hemostasis and completing of the angiographic procedures.     

Effect of Dietary Fatty Acid Composition on Th1/Th2 Polarization in Lymphocytes

Background: It has become increasingly clear that polyunsaturated fatty acids (PUFAs) have immunomodulatory effects. However, the intake of these fatty acids used in animal studies often greatly exceeds dietary human intake. Whether differences in the composition of fatty acids that are consumed in amounts consistent with normal dietary intake can influence immune function remains uncertain. Methods: We manufactured 3 types of liquid diet, related to modified fatty acid composition (ω‐6/ω‐3 = 0.25, 2.27 and 42.9), but excluding eicosapentaenoic acid and docosahexaenoic acid, based upon a liquid diet used clinically in humans. We assessed CD3‐stimulated cytokine production of splenocytes in female BALB/c mice (n = 4 per group) fed 1 of 3 liquid diets for 4 weeks. We also measured the cytokine production of peripheral blood mononuclear cells stimulated with phorbol myristate acetate and ionomycin in humans at the end of a 4‐week period of consumption of 2 different liquid diets (ω‐6/ω‐3 = 3 and 44). Results: We found that the ratio of interfero ω‐γ (IFN‐γ) / interleukin‐4 (IL‐4) was significantly higher in mice fed theω ‐3 rich diet than in others. In humans, IFN‐γ / IL‐4 was significantly higher after the ω‐3 versus the ω‐6 enhanced diet. Conclusions: Differences in the composition of ω‐3 andω ‐6 PUFAs induces a shift in the Th1/Th2 balance in both mouse and human lymphocytes, even when ingested in normal dietary amounts. An ω‐3 rich diet containing α‐linolenic acid modulates immune function.     

Changes in molecular markers of hemostatic and fibrinolytic activation under various sampling conditions using vacuum tube samples from healthy volunteers

Molecular makers such as thrombin-antithrombin complex (TAT), prothrombin fragment 1 + 2 (F1 + 2), soluble fibrin (SF), and D-dimer, are useful markers in the diagnosis and assessment of various thrombotic conditions. These markers are measured in plasma after blood sampling. Difficult blood sampling is known to falsely elevate plasma TAT levels. However, it is not known exactly why this occurs. In the present study, we examined how levels of molecular markers of haemostatic and fibrinolytic activation change under various sampling conditions using vacuum tube samples from healthy volunteers.When blood was sampled continuously by taking 10 consecutive vacuum tube samples following application of a tourniquet, blood sampling resulted in an accurate assessment of these molecular makers.When blood was sampled continuously by taking vacuum tube samples every one minute over a total of 9 minutes to investigate possible changes in the levels of the molecular markers over time, plasma levels of TAT, SF, and F1 + 2 gradually increased with time. Plasma levels of TAT, F1 + 2, and SF increased beyond the normal range over the course of nine minutes. When blood was sampled using three alternative methods, which varied in terms of the duration of needle puncture (sampling B), duration of tourniquet use (sampling C), or both (sampling A), plasma TAT and SF levels were significantly increased with all three methods, compared to control samples. Plasma F1 + 2 levels were significantly increased with sampling methods A and B, compared to control samples, but not with sampling method C. On the other hand, plasma D-dimer levels were not significantly altered by any of the sampling methods.In conclusion, the results suggest that molecular markers of haemostatic and fibrinolytic activation, except for D-dimer, may be affected by sampling method, particularly the duration of needle puncturing. Therefore, care needs to be taken when using TAT, F1 + 2, and SF levels to diagnose and estimate activation of the coagulation system.     

A dopamine receptor antagonist L-745,870 suppresses microglia activation in spinal cord and mitigates the progression in ALS model mice

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by a selective loss of motor neurons in the motor cortex, brainstem, and spinal cord. It has been shown that oxidative stress plays a pivotal role in the progression of this motor neuron loss. We have previously reported that L-745,870, a dopamine D4 receptor antagonist, selectively inhibits oxidative stress-induced cell death in vitro and exerts a potent neuroprotective effect against ischemia-induced neural cell damage in gerbil. To investigate the efficacy of L-745,870 in the treatment of ALS, we here conducted a chronic administration of L-745,870 to transgenic mice expressing a mutated form of human superoxide dismutase gene (SOD1^H46R); a mouse model of familial ALS, and assessed whether the mice benefit from this treatment. The pre-onset administration of L-745,870 significantly delayed the onset of motor deficits, slowed the disease progression, and extended a life span in transgenic mice. These animals showed a delayed loss of anterior horn cells in the spinal cord concomitant with a reduced level of microglial activation at a late symptomatic stage. Further, the post-onset administration of L-745,870 to the SOD1^H46R transgenic mice remarkably slowed the disease progression and extended their life spans. Taken together, our findings in a rodent model of ALS may have implication that L-745,870 is a possible novel therapeutic means to the treatment of ALS.     

First Turkish case of Bernard-Soulier syndrome associated with GPIX N45S

Bernard-Soulier syndrome (BSS) is a rare bleeding disorder characterized by giant platelets, thrombocytopenia, and a prolonged bleeding time. It is caused by homozygous defects in the glycoprotein (GP) Ib/IX/V complex, which is the receptor for the von Willebrand factor. We examined a Turkish patient with suspected BSS to identify a molecular basis. Flow cytometric analysis revealed that platelet GPIb alpha and GPIX expression was markedly reduced and DNA sequence analysis showed a homozygous N45S missense mutation in the GPIX gene. Haplotype analysis revealed that the family had the same disease haplotype associated with the GPIX N45S commonly found in Northern European BSS. This is the first non-Caucasian Turkish BSS case due to GPIX N45S and is likely the result of a recurrent mutational event.     

Living donor liver transplantation in a patient with giant hepatic hemangioma complicated by Kasabach-Merritt syndrome: Report of a case

We herein present a case of unresectable giant hepatic hemangiomas with Kasabach-Merritt syndrome which was successfully treated by living donor liver transplantation using a left lobe graft. The patient was a 45-year-old woman who complained of abdominal distension. Two sessions of transarterial embolization were performed, but failed to reduce the size of the tumor. The hepatic tumors were thus judged untreatable and the only option for a cure was to offer living donor liver transplantation, because of the tumor size, its location, and the association with Kasabach-Merritt syndrome. A left lobe graft with the middle hepatic vein donated by her 47-year-old brother was transplanted under venovenous bypass. The postoperative course of the recipient was complicated by small-for-size graft syndrome, which developed after episodes of acute cellular rejection on postoperative day 8 and sepsis on day 31. The patient successfully recovered from the complications and was discharged on day 72, and she remains well at 10 months after transplantation. In conclusion, living donor liver transplantation was found to be an effective option for the treatment of a patient with unresectable giant hepatic hemangiomas complicated by Kasabach-Merritt syndrome.     

Smoking affects prognosis after lung cancer surgery

Purpose To study the effects of smoking on the postoperative outcome of lung cancer surgery. Methods The subjects were 571 patients who underwent surgery for primary lung cancer. The patients were divided into the following groups according to their smoking history: a nonsmoker group (n = 218), a former smoker group (n = 140), and a current smoker group (n = 213). Results The 5-year survival rates were 56.2%, 40.9%, and 34.0% in the nonsmoker, former smoker, and current smoker groups, respectively. These differences were significant. According to a multivariable analysis, smoking was a significant factor affecting the postoperative prognosis of patients undergoing surgery for lung cancer. In analyzing the causes of death, there were more deaths caused by other diseases such as multiple organ cancer, respiratory disorder, cardiovascular disease, and surgery-related events in the former smoker and current smoker groups than in the nonsmoker group. Conclusions Smoking was significantly predictive of a poor prognosis after lung cancer surgery.