Inspiratory capacity and forced expiratory volume in the first second in exacerbation of chronic obstructive pulmonary disease

Object: Periodic exacerbations of symptoms are the major cause of morbidity, mortality and health care costs in patients with chronic obstructive pulmonary disease (COPD). Dyspnea is the major factor affecting the comfort of patients in the exacerbation of COPD. In this study, we aimed to compare the value of forced expiratory volume in the first second (FEV₁) and inspiratory capacity (IC) measured before and after treatment in exacerbations and in the improvement in dyspnea. Methods: Eighty‐seven patients (male/female, 80/7; mean age, 63 ± 7) with COPD exacerbation were included in this study. All subjects underwent spirometric tests on the first day and at the end of treatment. The subjects were asked to quantify the sensation of dyspnea that was described to them as a nonspecific discomfort associated with the act of breathing. The patients quantified dyspnea by pointing to a score on a large Borg scale from 0 to 10 arbitrary units. In the beginning and at the end of treatment, forced vital capacity (FVC), FEV₁, forced expiratory flow rate between 25% and 75% of FVC (FEF25–75), peak expiratory flow rate (PEF), IC and Borg score (BS) values were compared. Results: After treatment of COPD exacerbations, FEV₁, FEF25–75, PEF and IC significantly increased, and the BS significantly decreased compared to the initial values. The increase in IC was more significantly correlated with the improvement in BS compared with FEV₁. Admission and discharge day BS was negatively correlated with FEV₁, FEF25–75 and IC. Conclusion: We have shown a more dramatic improvement in IC compared with FEV₁ in patients treated as a result of acute exacerbation of COPD. These data suggest that IC may be more useful than FEV₁ during acute exacerbation of COPD. Moreover, IC better reflects the severity of dyspnea in these patients. Please cite this paper as: Yetkin O and Gunen H. Inspiratory capacity and forced expiratory volume in the first second in exacerbation of chronic obstructive pulmonary disease. The Clinical Respiratory Journal 2008; 2: 36–40.     

Melatonin ameliorates oxidative organ damage induced by acute intra-abdominal compartment syndrome in rats

Acutely increased intra-abdominal pressure (IAP) can lead to multiple organ failure. As blood flow to intra-abdominal organs is reduced by high venous resistance, ischemia-reperfusion (I/R) injury plays an important role in the pathogenesis of abdominal compartment syndrome (ACS) following IAP. Melatonin, a secretory product of the pineal gland, is known to have free radical scavenging and antioxidative properties in several oxidative processes. The objective of this study was to examine the potential protective properties of melatonin on the oxidative organ damage in a rat model of ACS. Under ketamine anesthesia, an arterial catheter was inserted intraperioneally (i.p.) and using an aneroid manometer connected to the catheter, IAP was kept at 20 mmHg (ischemia group; I) for 1 hr. In the ischemia/reperfusion (I/R) group, pressure applied for an hour was decompressed and a 1-hr reperfusion period was allowed. In another IR group, melatonin was administered (10 mg/kg, i.p.) immediately before the decompression of IAP. The results demonstrate that tissue levels of malondialdehyde (MDA) and myeloperoxidase activity (MPO; index of tissue neutrophil infiltration) were elevated, while glutathione (GSH; a key to antioxidant) levels were reduced in both I and I/R groups (P < 0.05-0.001). Melatonin treatment in I/R rats reversed these changes (P < 0.01-0.001). Moreover, melatonin given to the I/R group reduced the elevations in serum aspartate aminotransferase, alanine aminotransferase and blood urea nitrogen levels and abolished the increase in serum creatinine levels. Our results indicate that melatonin, because of antioxidant and free radical scavenging properties, ameliorates reperfusion-induced oxidative organ damage. In conclusion, the results of the present study suggest that the therapeutic value of melatonin as a 'reperfusion injury-limiting' agent must be considered in ACS.     

Severe mitral regurgitation may prevent mural thrombus formation within the left ventricle with systolic dysfunction

The protective effect of severe mitral regurgitation (MR) against left atrial thrombus formation has been well documented. It was also proposed that severe MR may prevent thrombus formation within the left ventricle (LV) with systolic dysfunction. Therefore, we investigated whether ischemic MR prevents thrombus formation within the LV in patients with systolic dysfunction. The study population was comprised of 1313 patients (1133 males, 180 females, age 56+/-18) with ischaemic LV dysfunction documented by coronary angiography and left ventriculography. None of the patients had a history of chronic anticoagulation. Epicardial coronary arteries were normal in 91 patients, and single-vessel, two-vessel, and triple-vessel disease were detected in 328, 330, and 564 patients, respectively. Left ventricular thrombus and severe MR were detected in 191 (14.5%) and 125 (9.5%) patients, respectively. Overall incidence of LV thrombus was lower in patients with severe MR than in patients without severe MR (4% vs 15.6%, OR: 0.2, P<0.001). Severe MR compared with absence of severe MR was associated with a lower incidence of LV thrombus both in patients with ischemic dilated cardiomyopathy (6.8% vs 34.2%, OR: 0.19, P<0.001), and in patients with aneurysm (3% vs 18%, OR: 0.14, P<0.0001) involving anterolateral, septal and/or apical LV segments. A similar trend without statistical significance was also observed in patients with dyskinesia (4.7% vs 16%, OR: 0.26, P=0.1) related to anterolateral, septal and/or apical LV segments. However, MR had no impact on the incidence of LV thrombus in patients with aneurysm or dyskinesia related to posterior and/or inferior segments (3.7% vs 3%, OR: 1.2, P>0.05). In conclusion, severe MR seems to prevent LV mural thrombus formation in patients with ischemic dilated cardiomyopathy, and in patients with aneurysm related to anterolateral, septal, and/or apical LV segments. This relative risk reduction may be associated with diastolic volume overloading due to severe MR which may overcome stagnation and a procoagulant state within the LV with severe systolic dysfunction.     

Protective effects of melatonin against spinal cord injury induced oxidative damage in rat kidney: A morphological and biochemical study

Spinal cord injury (SCI) induced oxidative stress affects multiple organ systems including the kidney. We studied the possible protective effects of melatonin on SCI-induced oxidative damage in renal tissues of rats. Wistar albino rats (n = 24) were exposed to SCI and divided into vehicle- or melatonin-treated SCI groups. Melatonin was administred intraperitoneally at a dose of 10 mg/kg for seven days. Renal tissues were investigated by light and electron microscopy. Furthermore, tissue malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and superoxide dismutase (SOD) activities were also determined. In the vehicle-treated SCI group, the renal histology was disturbed compared to controls, whereas the melatonin-treated SCI group showed significantly reduced degeneration of renal tissue as seen by both light and electron microscopy. MDA levels, MPO and SOD activities were increased and GSH levels were decreased in the vehicle-treated SCI group compared to controls. On the other hand, decreased MDA levels and MPO activities and increased GSH levels were observed in the melatonin-treated SCI group compared to vehicle-treated SCI group. These results showed that experimentally induced SCI caused oxidative stress in the rat kidney, whereas melatonin treatment reduced oxidative stress, suggesting that it may be used as a complementary therapy of renal problems occurring following SCI.     

Shell-core bi-layered scaffolds for engineering of vascularized osteon-like structures

Bottom-up assembly of osteon-like structures into large tissue constructs represents a promising and practical strategy toward the formation of hierarchical cortical bone. Here, a unique two-step approach, i.e., the combination of electrospinning and twin screw extrusion (TSE) techniques was used to fabricate a microfilament/nanofiber shell–core scaffold that could precisely control the spatial distribution of different types of cells to form vascularized osteon-like structures. The scaffold contained a helical outer shell consisting of porous microfilament coils of polycaprolactone (PCL) and biphasic calcium phosphates (BCP) that wound around a hollow electrospun PCL nanofibrous tube (the core). The porous helical shell supported the formation of bone-like tissues, while the luminal surface of nanofibrous core enabled endothelialization to mimic the function of Haversian canal. Culture of mouse pre-osteoblasts (POBs, MC 3T3-E1) onto the coil shells revealed that coils with pitch sizes greater than 135 μm, in the presence of BCP, favored the proliferation and osteogenic differentiation of POBs. The luminal surface of PCL nanofibrous core supported the adhesion and spreading of mouse endothelial cells (ECs, MS-1) to form a continuous endothelial lining with the function similar to blood vessels. Taken together, the shell–core bi-layered scaffolds with porous, coil-like shell and nanofibrous tubular cores represent a new scaffolding technology base for the creation of osteon analogs.     

Implementation of a Software Distribution Intervention to Improve Workload Balance in an Academic Pediatric Radiology Department

Journal of Digital Imaging - In our pediatric radiology department, radiographs (XR) are the shared responsibility of the body section and interpreted in addition to modality or site-specific...     

Comparison of protracted infusion 5-fluorouracil and capecitabine in adjuvant chemoradiotherapy for rectal cancer

BACKGROUND/AIMS: 5-Fluorouracil-based chemoradiotherapy is the most widely used treatment modality in the adjuvant treatment of rectal cancer. Capecitabine represents a valuable alternative to 5-Fluorouracil in this situation. METHODOLOGY: Patients with stage II and stage III rectal adenocarcinoma, who were included in this analysis, received adjuvant chemoradiotherapy consisting of external-beam radiotherapy (50.4-54Gy) either with 5-Fluorouracil at a median dose of 300 mg/m2/day by protracted venous infusion for 5 days a week, or capecitabine at a median dose of 1650 mg/m2/day for 5 days a week after surgery. The data concerning the toxicity and the efficacy of the treatments were compared in patients treated with 5-Fluorouracil- and capecitabine-based chemoradiotherapy. RESULTS: Forty-three patients received 5-Fluorouracil, and 24 patients received capecitabine during adjuvant radiotherapy. Although there were no differences between the groups in terms of toxicity rates, distant metastasis-free survival, disease-free survival, and overall survival rates; a trend for improved loco-regional recurrence-free survival rate was observed in the capecitabine arm (p = 0.063). CONCLUSIONS: Capecitabine is at least as effective as 5-Fluorouracil in the postoperative treatment of rectal adenocarcinoma. Considering the trend for improved loco-regional recurrence-free survival rate in the capecitabine arm, it seems that the drug exerts better synergy with radiotherapy in this situation.