Surveillance and oseltamivir resistance of human influenza a virus in Turkey during the 2007–2008 season

Monitoring the activity of influenza viruses is important for establishing the circulating types and for detection of the emergence of novel sub‐types and antiviral resistant strains. This is the first report from Turkey on the surveillance and oseltamivir resistance of influenza viruses in 2007–2008. Five hundred twenty‐four nasal swabs were tested from different geographical regions in Turkey during November 2007–April 2008. One hundred sixty‐three (31%) samples were positive for influenza viruses of which 111 (68%) were influenza A, 52 (31%) influenza B using an immuno‐capture ELISA. Forty isolates were selected at random from influenza A positive samples and grown in MDCK cell cultures. The supernatant of the cell cultures was used for RNA extraction followed by RT‐PCR to detect the sub‐types. Sub‐typing revealed all samples as A/H1N1. The N1 gene segment of 30 A/H1N1 samples was sequenced in part, from the 201st to 365th residue, which included the critical region for oseltamivir resistance. Then resulting sequences were analyzed with oseltamivir sensitive and resistant strains obtained from National Center for Biotechnology Information (NCBI) GenBank by CLC Main Workbench Software. H275Y (H274Y according to N2 numbering) mutation, which is known to confer resistance to oseltamivir, was detected in 6 out of 30 (20%) H1N1 isolates from four cities (Istanbul, Bursa, Ankara, and Izmir). The D354G mutation was observed in all oseltamivir resistant H1N1 isolates but not in the oseltamivir sensitive isolates. Assay of neuraminidase activity revealed that these isolates were resistant to oseltamivir, but sensitive to zanamivir. J. Med. Virol. 81:1645–1651, 2009. © 2009 Wiley‐Liss, Inc.     

Determination of nitric oxide synthase activity and apoptosis of germ cells in different obstruction models

We aimed to determine the changes of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) immunoreactivity and apoptosis after proximal and distal obstruction models on ipsilateral and contralateral testicular tissues. Male albino Wistar rats were randomly divided into three groups (n=30): a control group which underwent sham operations (n=10), a unilateral vasal ligation (n=10) and a unilateral epididymal ligation group (n=10). iNOS and eNOS distribution and apoptosis were studied in both ipsilateral and contralateral testes using quantitative immunohistochemistry. Nitric oxide synthase activity was significantly affected in ipsilateral and contralateral testes cells after vasal and epididymal ligation. eNOS immunoreactivity increased markedly after ipsilateral vasal ligation (ILVL). Degeneration-related changes were also associated with changes in apoptotic rate. Analysis using the terminal dUTP nick end-labeling TUNEL method revealed that apoptotic cell numbers significantly increased after ILVL. p53 and bcl-2 immunoreactivity increased in both experimental groups compared with the sham-operated group. Changes in iNOS and eNOS immunolocalisation were strongly associated with cell damage, because germ cell degeneration was more prominent in the ILVL group. Altered p53 immunolocalisation was also associated with cell degeneration, and a rise in bcl-2 immunoreactivity might be considered to reflect a protective mechanism in the testis. These cellular changes could enlighten understanding of the interaction between testicular functioning and damage.     

Comparision of the effects of subtenon’s and subconjunctival anesthesia on retroorbital hemodynamics

The aim of the study was to compare retroorbital blood flow hemodynamics between subconjunctival and sub-Tenon’s anesthesia. This was a prospective, blinded study and included 80 cases. Patients were monitored and treated in the First Ophthalmology Clinic, Ataturk Training and Research Hospital, Turkey. Sub-Tenon’s anesthesia was performed in 42 cases, and subconjunctival anesthesia was performed in 38 cases. Color Doppler imaging to measure ocular blood flow parameters was performed preoperatively and 21 days after cataract operation in each case. Preoperative and postoperative values of resistivity and pulsatility indices in the ophthalmic, central retinal, and short posterior ciliary arteries were compared. Postoperative mean blood flow velocity measurements of ophthalmic artery were not statistically different between the subconjunctival anesthesia group and the sub-Tenon’s anesthesia group (49.63 ± 14.00 vs. 45.85 ± 13.41; P=0.389). Postoperative RI values were higher in the Subtenon’s anesthesia group than in the subconjunctival anesthesia group, but the difference between two groups was not statistically significant (0.81 ± 0.14 vs. 0.74 ± 0.08; P=0.079). The postoperative pulsatility index of the ophthalmic artery, RI of ophthalmic artery, pulsatility index of the central retinal artery, RI of the central retinal artery, and pulsatility index of the posterior ciliary arteries were not significantly different between the subconjunctival and sub-Tenon’s anesthesia groups. In conclusion, the study suggests that postoperative retroorbital blood flow hemodynamics are the same following sub-Tenon’s and subconjunctival anesthesia.     

Effects of subacute exposure of dichlorvos at sublethal dosages on erythrocyte and tissue antioxidant defense systems and lipid peroxidation in rats

In this study, the effects of dichlorvos (DIC) at sublethal concentration on malondialdehyde (MDA) content and antioxidant defense system (ADS) such as reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), and glutathione-S-transferase (GST) in various tissues of rats exposed to 0.0225 and 0.0450 millimole (mmol) DIC in drinking water were administered orally to rats ad libitum for 28 days continuously. MDA significantly increased in all the tissues except in the lungs of rats treated with both dosages of DIC. With regard to the ADS, GR significantly decreased in the erythrocytes whereas it did not change in the other tissues with two dosages of DIC. SOD activity significantly increased in the all tissues treated with both dosages of DIC. GST activity significantly increased in all the tissues except in the erythrocytes, spleen, and lungs treated with 0.0225mmol. Meanwhile, GSH depletion in the liver and heart of rats treated with 0.0225mmol and all the tissues except in the brain and kidney of rats treated with 0.0450mmol of DIC were found to be significant. The observations presented led us to conclude that the administrations of DIC promote MDA content and fluctuate in the ADS in rats during the exposure.     

Effect of different intra-abdominal pressure levels on QT dispersion in patients undergoing laparoscopic cholecystectomy

Background

Hemodynamic changes caused by carbon dioxide (CO₂) insufflation occur frequently in patients who undergo laparoscopic surgery. One indicator of these changes is corrected QT dispersion (QTcd), an index of myocardial function. Prolongation of QTcd has been associated with cardiovascular morbidity and mortality. We compared the effects of high-pressure (15 mmHg) and low-pressure (7 mmHg) CO₂ pneumoperitoneums on the QT interval, the rate-corrected QT interval (QTc), the QT dispersion (QTd), and the corrected QT dispersion (QTcd) during laparoscopic cholecystectomy.

Methods

Twenty consecutive patients were in a low-pressure pneumoperitoneum group and 32 were in a high-pressure pneumoperitoneum group. A 12-lead electrocardiogram was used to monitor cardiac variables. In all patients, serial electrocardiograms were recorded before anesthesia induction (baseline), immediately after the pneumoperitoneum had been created, every 15 minutes during CO₂ insufflation, and 5 minutes after deflation. Two observers measured the QT intervals independently, and the QTcd was calculated using Bazett’s formula.

Results

The QT interval and the QTc interval did not change significantly during the study in either group. The QTd and QTcd in the high-pressure pneumoperitoneum group increased significantly during CO₂ insufflation and were significantly higher in the high-pressure pneumoperitoneum group compared with the low-pressure pneumoperitoneum group. Changes caused by CO₂ insufflation were reversible.

Conclusions

Statistically significant increases of QTd and QTcd, which are associated with an increased risk of arrhythmias and cardiac events, occur during CO₂ insufflation in both high-pressure and low-pressure pneumoperitoneums. QTd and QTcd were significantly higher in the high-pressure pneumoperitoneum group than they were in the low-pressure pneumoperitoneum group. QT interval changes were not related to anesthetic agents, surgical stress, hypercapnia, or duration of CO₂ insufflation. Increased intra-abdominal pressure may have caused these changes.     

The Effect of <Emphasis Type="Italic">N</Emphasis>ω-Nitro-<Emphasis Type="SmallCaps">l</Emphasis>-Arginine Methyl Ester and <Emphasis Type="SmallCaps">l</Emphasis>-Arginine on Lung Injury Induced by Abdominal Aortic Occlusion–Reperfusion

Purpose

The aim of this study was to examine the effects of Nω-nitro-l-arginine methyl ester (l-NAME) and l-arginine on lung injury after aortic ischemia–reperfusion (IR).

Methods

Twenty-four Wistar-Albino rats were randomized into four groups (n = 6) as follows: Control (sham laparotomy), Aortic IR (30?min ischemia and 120?min reperfusion), l-Arginine (intraperitoneal 100?mg?kg<συπ>?1 live weight)+aortic IR, and l-NAME (intraperitoneal 10?mg?kg<συπ>?1 live weight)+aortic IR. In the lung specimens, the tissue levels of malondialdehyde (MDA), vascular endothelial growth factor (VEGF), and nitric oxide (NO) were measured and a histological examination was done.

Results

Aortic IR increased MDA, VEGF, and NO. l-Arginine further significantly increased MDA and NO, and decreased VEGF (P < 0.05 vs aortic IR). l-NAME significantly decreased MDA and NO (P < 0.05 vs l-arginine+aortic IR) and increased VEGF (P < 0.05 vs other groups). A histological examination showed the aortic IR to significantly increase (P < 0.05 vs control) while l-arginine also further increased (P > 0.05 vs aortic IR), whereas l-NAME caused a significant decrease in pulmonary leukocyte infiltration (P < 0.05 vs aortic IR).

Conclusions

Our results indicate that l-arginine aggravates the lung injury induced by aortic IR, while l-NAME attenuates it.