Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats.

BACKGROUND: Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R. MATERIALS AND METHODS: A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group. RESULTS: Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group's lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group. CONCLUSIONS: During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced.

Investigation of surfactant protein-D and interleukin-6 levels in patients with blunt chest trauma with multiple rib fractures and pulmonary contusions: a cross-sectional study in Black Sea Region of Turkey.

OBJECTIVE: Multiple rib fractures (RFs) and pulmonary contusions (PCs), with resulting systemic lung inflammation, are the most common injuries caused by blunt chest trauma (BCT) in motor vehicle accidents. This study examined levels of the inflammation marker interleukin (IL)-6 and those of the acute-phase reactant surfactant protein (SP)-D in patients with BCT. DESIGN: Prospective, cross-sectional, observational study. SETTING: Single-centre, tertiary care hospital in the Black Sea Region of Turkey. PARTICIPANTS: The study included 60 patients with BCT who were hospitalised in our thoracic surgery department. PARAMETERS MEASURES: The SP-D and IL-6 serum levels of patients with RFs (two or more RFs) (n=30) and patients with PCs (n=30) were measured after 6 hours, 24 hours and 7 days, and compared with those of age-matched and gender-matched healthy participants. RESULTS: The 6-hour serum SP-D levels of the RFs (p=0.017) and PCs (p<0.001) groups were significantly higher than those of the healthy controls. The 24-hour and 7-day SP-D levels of both groups were also higher than the control group. The serum IL-6 levels of both groups were significantly higher than those of the control group. We have found Injury Severity Score to be independently related to 6-hour IL-6 (ß=1.414, p<0.001) and 24-hour IL-6 levels (ß=1.067, p<0.001). The development of complications was independently related to 6-hour SP-D level (ß=0.211, p=0.047). CONCLUSIONS: RFs and PCs after BCT lead to local and systemic inflammation due to lung injury. The levels of the systemic inflammation marker IL-6 and those of the acute-phase reactant SP-D were elevated in the present study. The SP-D level may be used as a marker in the follow-up of BCT-related complications.

The Protective Effect of Adalimumab on Renal Injury in a Model of Abdominal Aorta Cross-Clamping.

BACKGROUND: Adalimumab (ADA) is a potent inhibitor of tumor necrosis factor (TNF-α). ADA treatment suppresses proinflammatory cytokines, leading to a decrease or inhibition of the inflammatory process. OBJECTIVES: The aim of this study was to investigate the possible protective effects of ADA on oxidative stress and cellular damage on rat kidney tissue after ischemia/reperfusion (I/R). MATERIAL AND METHODS: A total of 30 male Wistar albino rats were divided into three groups: control, I/R, and I/R plus ADA (I/R + ADA); each group comprised 10 animals. The control group underwent laparotomy without I/R injury. After undergoing laparotomy, I/R groups underwent two hours of infrarenal abdominal aortic cross ligation, which was followed by two hours of reperfusion. ADA (50 mg/kg) was administered as a single dose, intraperitoneally, to the I/R + ADA group, 5 days before I/R. RESULTS: The I/R group's TNF-α (1150.9 ± 145.6 pg/mg protein), IL-1ß (287.0 ± 32.4 pg/mg protein) and IL-6 (1085.6 ± 56.7 pg/mg protein) levels were significantly higher than those of the control (916.1 ± 88.7 pg/mg protein, p = 0.003; 187.5 ± 37.2 pg/mg protein, p < 0.001; 881.4 ± 57.1 pg/mg protein, p < 0.001, respectively) and I/R + ADA groups (864.2 ± 169.4 pg/mg protein, p = 0.003; 241.4 ± 33.4 pg/mg protein, p = 0.010; 987.7 ± 66.5 pg/mg protein, p = 0.004, respectively). To date, a few histopathological changes have been reported regarding renal I/R injury in rats due to ADA treatment whereas I/R caused severe histopathological injury to kidney tissue. CONCLUSIONS: ADA treatment significantly attenuated the severity of kidney I/R injury, inhibiting I/R-induced oxidative stress and renal damage. Because of its anti-inflammatory and antioxidant effects, ADA pretreatment may have protective effects on experimental kidney injury.

The protective effect of infliximab against carbon tetrachloride-induced acute lung injury.

OBJECTIVES: Carbon tetrachloride (CCl4) causes pulmonary toxicity. Infliximab (Ib) is a potent inhibitor of tumor necrosis factor-alpha (TNF-α). We aimed to investigate whether Ib has a protective effect on CCl4 induced lung injury. MATERIALS AND METHODS: Rats were divided into control, CCl4, and CCl4+Ib groups. A single dose of 2 ml/kg CCI4 was administered to CCI4 group and a single dose of 7 mg/kg Ib was given to CCl4+Ib group 24 hr before applying CCI4. RESULTS: TNF-α, malondialdehyde (MDA), nitric oxide (NO) and caspase-3 levels of the CCl4 group were markedly higher than both the control and CCl4+Ib groups. The CCI4+Ib group had lower histopathological injury than the CCl4 group. CONCLUSION: Ib as a strong TNF-α blocker decreases the production of proinflammatory cytokines, MDA, and oxidative stress leading to a protective effect against CCl4 induced lung tissue injury.

Efectos protectores de infliximab sobre el daño pulmonar inducido por metotrexato / Protective Effects of Infliximab on Lung Injury Induced by Methotrexate

Introducción: El metotrexato (MTX) se emplea para tratar el cáncer, varias formas de artritis y otras patologías reumáticas, pero puede causar toxicidad pulmonar debido a la producción de radicales libres del oxígeno y varias citocinas. Infliximab (IB) es un potente inhibidor del factor de necrosis tumoral-alfa (TNF-alfa) e inhibe también la liberación de endotelina-1 (ET-1). Nos propusimos investigar si IB reduce el daño pulmonar inducido por una sobredosis de MTX. Método: Las ratas se dividieron en 3 grupos de 8 animales. Al grupo control solamente se le administró solución salina. Al grupo MTX se le administró una dosis intraperitoneal de 20 mg/kg de MTX. Al grupo de MTX + IB (MI) se le administraron 7 mg/kg de IB. Tres días después de la administración de IB se administraron 20mg/kg de MTX. Todas las ratas se sacrificaron 5días después de la administración de MTX. Resultados: Las concentraciones de TNF-alfa, ET-1, malondialdehído (MDA), mieloperoxidasa (MPO) y caspasa-3 fueron significativamente más altas en el grupo MTX que en el grupo control: TNF-alfa (p < 0,001), ET-1 (p < 0,001), MDA (p < 0,001), MPO (p < 0,001) y caspasa-3 (p < 0,001) y en el grupo MI: TNF-alfa (p < 0,009), ET-1 (p < 0,001), MDA (p < 0,047), MPO (p < 0,007) y caspasa-3 (p < 0,003). El grupo MI mostró menos daño histopatológico en el tejido pulmonar que en el grupo MTX. Conclusión: La sobredosis de MTX induce la liberación de citocinas y la formación de especies reactivas de oxígeno, además de una mayor secreción de ET-1 que provoca daño pulmonar. IB es un agente proinflamatorio potente, bloquea el TNF-alfa, puede reducir la liberación de ET-1 y el estrés oxidativo y mostrar importantes efectos protectores del tejido pulmonar frente al daño causado por una sobredosis de MTX

Introduction: Methotrexate (MTX) is used to treat cancers, several forms of arthritis and other rheumatic conditions, although MTX may cause pulmonary toxicity related to the production of free oxygen radicals, various cytokines. Infliximab (IB) with its potent effect on tumor necrosis factor-alpha (TNF-alfa) inhibition also inhibits the release of endothelin-1 (ET-1). We aimed to investigate whether IB reduces pulmonary damage induced by an overdose of MTX. Method: The rats were divided into 3 groups of 8 animals. The control group was given only saline. One dose of 20 mg/kg MTX intraperitoneal was administered in the MTX group. IB 7 mg/kg was given to the MTX + IB (MI) group. Three days after IB was administered, 20 mg/kg MTX was given. Five days after MTX was administered, all rats were sacrificed. Results: The TNF-α, ET-1, malondialdehyde (MDA), myeloperoxidase (MPO) and caspase-3 levels in MTX group were significantly higher than in control groups of TNF- alfa (P = .001), ET-1 (P = .001), MDA (P = .001), MPO (P = .001) and caspase-3 levels (P = .001) and MI groups of TNF-alfa (P=.009), ET-1 (P = .001), MDA (P = .047), MPO (P = .007) and caspase-3 levels (P = .003). The MI group had less histopathological damage in lung tissue than the MTX group. Conclusion: Overdose of MTX leads to cytokine release and the formation of reactive oxygen species in addition to increased ET-1 secretion release that causes lung damage. IB, as a potent proinflammatory agent, TNF-alfa blocker, can decrease ET-1 release and oxidative stress, it may show significant protective effects in lung tissue against damage caused by MTX overdose

Clinical potential of resistin as a novel prognostic biomarker for cellulitis.

Cellulitis is an acute, subacute or chronic inflammation of the dermis and subdermal tissues, which is typically caused by bacteria, although other causes are possible. The present study aimed to evaluate the association between resistin levels and the recovery time of patients with cellulitis. In addition, the effect of resistin and insulin resistance on the prognosis of cellulitis was investigated. In total, 52 patients with cellulitis (male, 21; female, 31) and an age-matched group of 42 healthy individuals (male, 18; female, 24) were included in the study. The levels of serum resistin, fasting plasma glucose (FPG), homeostasis model assessment-insulin resistance (HOMA-IR), C-reactive protein (CRP) and other biochemical parameters were compared between the groups. The mean resistin levels in the cellulitis and control groups were 9.4±5.3 and 5.8±3.1 ng/ml, respectively. The levels of resistin, FPG, HOMA-IR and CRP were significantly higher in the cellulitis group compared with the control group (P<0.001). Furthermore, the mean recovery time of the patients with cellulitis was 21.2±5.6 days. Thus, increased levels of resistin (P=0.002) and HOMA-IR (P=0.005) could be used as predictive factors for the recovery time. The enhanced levels of resistin and HOMA-IR were shown to correlate with the high CRP levels in the cellulitis group. Therefore, the results indicated that increased levels of resistin may function as a prognostic marker for cellulitis.

Protective Effects of Infliximab on Lung Injury Induced by Methotrexate.

INTRODUCTION: Methotrexate (MTX) is used to treat cancers, several forms of arthritis and other rheumatic conditions, although MTX may cause pulmonary toxicity related to the production of free oxygen radicals, various cytokines. Infliximab (IB) with its potent effect on tumor necrosis factor-alpha (TNF-α) inhibition also inhibits the release of endothelin-1 (ET-1). We aimed to investigate whether IB reduces pulmonary damage induced by an overdose of MTX. METHOD: The rats were divided into 3 groups of 8 animals. The control group was given only saline. One dose of 20mg/kg MTX intraperitoneal was administered in the MTX group. IB 7 mg/kg was given to the MTX+IB (MI) group. Three days after IB was administered, 20mg/kg MTX was given. Five days after MTX was administered, all rats were sacrificed. RESULTS: The TNF-α, ET-1, malondialdehyde (MDA), myeloperoxidase (MPO) and caspase-3 levels in MTX group were significantly higher than in control groups of TNF-α (P=.001), ET-1 (P=.001), MDA (P=.001), MPO (P=.001) and caspase-3 levels (P=.001) and MI groups of TNF-α (P=.009), ET-1 (P=.001), MDA (P=.047), MPO (P=.007) and caspase-3 levels (P=.003). The MI group had less histopathological damage in lung tissue than the MTX group. CONCLUSION: Overdose of MTX leads to cytokine release and the formation of reactive oxygen species in addition to increased ET-1 secretion release that causes lung damage. IB, as a potent proinflammatory agent, TNF-α blocker, can decrease ET-1 release and oxidative stress, it may show significant protective effects in lung tissue against damage caused by MTX overdose.

Is adalimumab protective in ischemia-reperfusion injury in lung?

OBJECTIVES: Increasing cytokines and reactive oxygen species (ROS) during ischemia reperfusion (I-R) leads to the lung damage. Adalimumab (Ada) is a potent tumor necrosis factor-alpha (TNF-α) inhibitor agent. We aimed to evaluate whether Ada would prevent the lung tissue from damage development over the I-R process. MATERIALS AND METHODS: Twenty seven Wistar albino male rats were divided into three groups (each group had 9 rats). To the control group, only laparotomy procedure was carried out. For I-R group, first infrarenal abdominal aorta was cross-clamped during 2 hr, and then reperfusion was performed for 2 hr. To I-R+Ada group, first a single dose of 50 mg/kg Ada was given intraperitoneally and 5 days later, same I-R procedure was carried out. RESULTS: Levels of TNF-α, malondialdehyde (MDA), myeloperoxidase (MPO), endothelin-1 (ET-1) and caspase-3 enzyme activity of I-R group were higher than that of both I-R+ Ada [TNF-α (P=0.021), MDA (P=0.029), MPO (P=0.012), ET-1 (P=0.036, caspase-3 (P=0.007), respectively] and control group [TNF-α (P=0.008), MDA (P<0.001), MPO (P=0.001), ET-1 (P<0.001), caspase-3 (P<0.001), respectively]. In I-R group, severe damage was detected by hematoxylin-eosin staining. This damage was found less severe in Ada treatment group. CONCLUSION: The release of cytokines and ET-1 in a large proportion after I-R injury, and generating of ROS in excessive quantity could cause severe damage in the lung tissue. Ada could be considered as a protective agent for lung tissue during I-R process.

A novel model approach for esophageal burns in rats: A comparison of three methods.

BACKGROUND: Corrosive esophageal injury causes serious clinical problems. We aimed to create a new experimental esophageal burn model using a single catheter without a surgical procedure. MATERIALS AND METHODS: We conducted the study with two groups of 12 male rats that fasted for 12 h before application. A modified Foley balloon catheter was inserted into the esophageal lumen. The control group was given 0.9% sodium chloride, while the experimental group was given 37.5% sodium hydroxide with the other part of the catheter. After 60s, esophagus was washed with distilled water. The killed rats were examined using histopathological methods after 28 days. RESULTS: In comparison with the histopathological changes experienced by the study groups, the control groups were observed to have no pathological changes. Basal cell degeneration, dermal edema, and a slight increase in the keratin layer and collagen density of submucosa due to stenosis were all observed in the group subjected to esophageal corrosion. CONCLUSION: A new burn model can thus, we believe, be created without the involvement of invasive laparoscopic surgery and general anesthesia. The burn in our experiment was formed in both the distal and proximal esophagus, as in other models; it can also be formed optionally in the entire esophagus.

Molecular characterisation and control of Acinetobacter baumannii isolates resistant to multi-drugs emerging in inter-intensive care units.

BACKGROUND: A nosocomial outbreak of Acinetobacter baumannii (AB) infections occurred among intensive care units (ICU) (surgery, medical, cardiovascular surgery, coronary unit) of Recep Tayyip Erdogan University Medical School (Rize, Turkey) between January 2011 and May 2012. The identification of isolates and clonal relation among them were investigated by molecular techniques. METHODS: A total of 109 AB isolates were obtained from 64 clinical materials from 54 ICU patients and 3 from the hands of healthcare workers (HCWs) of 42 environmental samples. The isolates were identified by 16S rDNA sequencing and OXA- specific PCR. The clonal relation between isolates was investigated by PFGE methods using ApaI restriction enzyme. RESULTS: All isolates were determined as AB by 16S rDNA sequencing and OXA-spesific PCR. While the blaOXA-51-like gene was amplified in all isolates, the blaOXA-23-like gene was amplified from 103 isolates. The PFGE pattern generated 9 pulsotypes and showed that the isolates from patients, HCWs, and the environment were genetically related. In 7 of these pulsotypes, there were 107 strains (98%) showing similar PFGE profiles that cannot be distinguished from each other, ranging from 2 to 53. The remaining 2 pulsotypes were comprised of strains closely associated with the main cluster. Two major groups were discovered with similarity coefficient of 85% and above. The first group consisted of 97 strains that are similar to each other at 92.7% rate, and the second group consisted of 12 strains that are 100% identical. CONCLUSIONS: The common utilization of the blood gas device among ICU was the reason for the contamination. AB strains can remain stable for a long period of time, although due to the disinfection procedures applied in hospitals, there is a small chance that the same clone might reappear and cause another epidemic. For that reason, the resistance profiles of the strains must be continuously followed with amplification-based methods, and these methods should be used to support the PFGE method in the short term.

On-call service of neurosurgeons in Germany: organization, use of communication services, and personal acceptance of modern technologies.

BACKGROUND: A significant proportion of acute care neurosurgical patients present to hospital outside regular working hours. The objective of our study was to evaluate the structure of neurosurgical on-call services in Germany, the use of modern communication devices and teleradiology services, and the personal acceptance of modern technologies by neurosurgeons. MATERIALS AND METHODS: A nationwide survey of all 141 neurosurgical departments in Germany was performed. The questionnaire consisted of two parts: one for neurosurgical departments and one for individual neurosurgeons. The questionnaire, available online and mailed in paper form, included 21 questions about on-call service structure; the availability and use of communication devices, teleradiology services, and other information services; and neurosurgeons' personal acceptance of modern technologies. RESULTS: The questionnaire return rate from departments was 63.1% (89/141), whereas 187 individual neurosurgeons responded. For 57.3% of departments, teleradiology services were available and were frequently used by 62.2% of neurosurgeons. A further 23.6% of departments described using smartphone screenshots of computed tomography (CT) images transmitted by multimedia messaging service (MMS), and 8.6% of images were described as sent by unencrypted email. Although 47.0% of neurosurgeons reported owning a smartphone, only 1.1% used their phone for on-call image communication. CONCLUSION: Teleradiology services were observed to be widely used by on-call neurosurgeons in Germany. Nevertheless, a significant number of departments appear to use outdated techniques or techniques that leave patient data unprotected. On-call neurosurgeons in Germany report a willingness to adopt more modern approaches, utilizing readily available smartphones or tablet technology.

Noncardiac Pulmonary Edema induced by Sitagliptin Treatment.

A 74-year-old male patient with type 2 diabetes mellitus admitted to the emergency department with the complaints of progressive breathlessness, dry cough, and swollen lower extremities. Our patient had type 2 diabetes mellitus and hypertension for 3 years. His HbA1c was not within the target range so sitagliptin was added to on-going therapy. After 1 week of starting sitagliptin therapy, even though the patient had not heart failure he applied to the emergency department with a complaint of dyspnea. The cardiovascular safety and efficacy of many anti-hyperglycemic agents such as sitagliptin, saxagliptin are unclear. Our case has shown that dipeptidyl peptidase 4 inhibitors may cause pulmonary edema. Hence, it should be used with cautious, especially in patients with heart failure.

Complications of metallic stent placement in malignant esophageal stricture and their management.

OBJECTIVE: At the present time, covered self-expandable metallic stent placement is the palliative treatment method for inoperable esophageal cancer. However, life-threatening early and late complications are seen related to esophageal stent placement. In this study, we discuss complications of esophageal stent placement with their management and present our own experience. METHODS: Between January 2000 and February 2009, 215 covered esophageal stent placements were performed in 174 inoperable esophageal cancer and/or esophagorespiratory fistula patients in the Department of Thoracic Surgery at the Ataturk University Hospital. RESULTS: Major complications related to stent placement developed in 24 patients (11 bleeding, 6 aspiration pneumonia, 3 tracheal compressions, 2 perforations, and 2 esophagorespiratory fistulas). Two hundred and thirty minor complications were observed among 174 patients (165 chest pain, 29 tumoral overgrowth, 17 stent migration, 6 gastroesophageal reflux, 3 failure in stent placement, 3 hiccup, 2 foreign body sensation, 2 failure in stent expansion, 1 tumor ingrowth, 1 granulation tissue formation, and 1 food bolus obstruction). Reintervention was required in 56 (32.2%) patients who experienced complications. Stent-related mortality was seen in 4 (2.3%) patients (2 aspiration pneumonia, 1 tracheal compression, and 1 esophagorespiratory fistula). One hundred sixty-two of 174 patients died during follow up. The mean survival time was 177.3+/-59.3 days (range: 2 to 993 d). CONCLUSIONS: The complication rate of self-expandable metallic stent placement is high in inoperable esophageal cancer patients. Although some of these complications are life threatening, many of them can be managed successfully with endoscopic reintervention.