OBSERVATION OF AN ISOKINETIC TEMPERATURE AND COMPENSATION EFFECT FOR HIGH TEMPERATURE CRUDE OIL FOULING

The initial fouling rates of four crude oils were determined at a nominal bulk temperature of 315 °C, an initial heated wall shear stress of 13 Pa, and initial surface temperatures between 375 and 445 °C. These initial fouling rates ranged from 1.3(10-6) to 7.8(10-5) m2 K/kJ. Corresponding Arrhenius plots were linear with the initial fouling rates passing through an isokinetic temperature of 407.5 °C. A plot of the natural logarithm of the preexponential factors (7.6(104) – 5.2(1015) m2 K/kJ) versus the apparent activation energies (128 – 269 kJ/mol) was also linear, confirming the validity of the isokinetic temperature and the presence of the compensation effect. Below the isokinetic temperature, the relative fouling rates were Crude Oil C \u3e Crude Oil A \u3e Crude Oil D \u3e Crude Oil B; above the isokinetic temperature, the relative fouling rates were reversed (Crude Oil B \u3e Crude Oil D \u3e Crude Oil A \u3e Crude Oil C). Chemical characterization of a fouling deposit suggested that the dominant fouling mechanism at these conditions was coking with significant contributions from sedimentation (iron sulfide) and corrosion (~340 μm/yr) of the 304 stainless steel test material

OBSERVATION OF AN ISOKINETIC TEMPERATURE AND COMPENSATION EFFECT FOR HIGH TEMPERATURE CRUDE OIL FOULING

The initial fouling rates of four crude oils were determined at a nominal bulk temperature of 315 °C, an initial heated wall shear stress of 13 Pa, and initial surface temperatures between 375 and 445 °C. These initial fouling rates ranged from 1.3(10-6) to 7.8(10-5) m2 K/kJ. Corresponding Arrhenius plots were linear with the initial fouling rates passing through an isokinetic temperature of 407.5 °C. A plot of the natural logarithm of the preexponential factors (7.6(104) – 5.2(1015) m2 K/kJ) versus the apparent activation energies (128 – 269 kJ/mol) was also linear, confirming the validity of the isokinetic temperature and the presence of the compensation effect. Below the isokinetic temperature, the relative fouling rates were Crude Oil C \u3e Crude Oil A \u3e Crude Oil D \u3e Crude Oil B; above the isokinetic temperature, the relative fouling rates were reversed (Crude Oil B \u3e Crude Oil D \u3e Crude Oil A \u3e Crude Oil C). Chemical characterization of a fouling deposit suggested that the dominant fouling mechanism at these conditions was coking with significant contributions from sedimentation (iron sulfide) and corrosion (~340 μm/yr) of the 304 stainless steel test material

Analysis of Blood Cultures in Major Burns in Tertiary Care Burn Unit in Oman

Objectives: In this study we review blood stream infections of major burns in a tertiary care burn unit to determine the most prevalent organisms in order to have a better empirical therapy protocol. Methods: This is a retrospective study where blood stream infection of major burns (>20% Total Body Surface Area) were analysed. Results:155 patients fulfilled the criteria. Median age was 33 years.  Median TBSA was 38%. 57.42% were males and 42.58% were females. Mortality was 25.16%. 50.9% of patients had positive blood culture. Expired patients had higher TBSA, Abbreviated Burns Severity Index score and earlier first positive blood culture. The most prevalent organisms grown from all blood cultures were Acinetobacter, staphylococci, Klebsiella, Enterococcus and pseudomonas. Candida is also commonly grown in blood cultures. All Acinetobacter species are always multidrug resistant. 8 of 14 patients had multidrug resistant Klebsiella.  There were only 4 patients who had Methicilin resistant Staphylococcus Aureus (MRSA) grown. The number of blood cultures samples taken ranged from 1 to 28 (median 6). First positive blood culture showed that Staphylococcus epidermidis   and Acinetobacter are the most common organisms. Conclusion: In conclusion multidrug resistant Acinetobcater has become the most predominant microorganism grown in blood cultures of major burns in our unit. Empirical therapy should include antibiotics that are effective against it to reduce the mortality. Keywords: Infection; Blood; Burn; Resistance; Antibiotics; Culture

Some fertility problems associated with Kuwaiti calcareous soil and brackish irrigation water

SIGLEAvailable from British Library Document Supply Centre- DSC:DX179854 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Effects of cyclooxygenase inhibitors on fracture healing and the reversibility of effects after short term treatment

PLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact [email protected] (MSD)--Boston University, Goldman School of Dental Medicine, 2005 (Restorative Sciences and Biomaterials).Includes bibliographical references: leaves 66-72.Introduction: Previous studies have suggested that both COX-2-specific (coxibs) and nonspecific anti-inflammatory drugs (NSAIDs) inhibit fracture healing. Because drug specificity, dose, and duration may influence fracture healing, and because patients with fractures require analgesia for only short periods of time after initial stabilization, we tested the hypothesis that the negative effects of these drugs on fracture healing would be reversible with short-term treatment. Materials and Methods: Two hundred fifty male Sprague Dawley rats underwent standard, closed mid diaphyseal femoral fracture. Immediately post fractures, animals were divided in groups for histomorphometry, mechanical testing, and PGE2 assay. Combinations of placebo, non-specific (ketorolac), COX 2 specific NSAID (valdecoxib) treatment were given at different doses and for different durations. For statistical analysis ANOVA, Fisher’s Exact Test, and multivariate analysis of variance at P[less than]0.05 were used. Results: In rats treated for 7 days, showed no significant differences in % of nonunions after 21 days (16% of ketorolac, 22% of valdecoxib, and 8% of vehicle-treated animals, p=0.47), nor after 35 days (5% of ketorolac , 0% of valdecoxib, and 9% of vehicle-treated, p= 1.0). In rats treated for 21 days, there were differences in % of nonunions after 21 days (13% of ketorolac, 36% of valdecoxib, and 4% of vehicle-treated,p =0.01), but the differences disappeared by 35 days (none in the ketorolac and valdecoxib groups, 5% in vehicle-treated, p=1.0). Torsional testing showed statistically significant diminishment in both stiffness and strength at 35 days post fracture for those animals treated for 21 days with the COX2 specific NSAID but there was no observable difference in mechanical strength in those animals treated for only 7 days. Histomoxphometry showed a strong correlation between non-union rate and percent cartilage in the calluses which is consistent with diminished mechanical stiffness of the calluses. Histological assessment further showed diminished marrow cellular contents in both 2 1 day non and specific NSAID treated tissues which was recovered if the drug was withdrawn at seven days. Analysis of PGE2 levels in the calluses showed that the non-specifc NSAID had 2 to 3 fold lower levels than the specific coxib and exhibited an increasing inhibition at progressively higher doses while the COX-2 specific NSAID did not show any dose dependency of inhibition over a log difference in oral doses. Conclusions: These data suggest COX2 specific NSAIDs delay fracture healing and the magnitude of the effect as measured by non-union in this study was related to the duration of treatment. Treated animals recover their healing capacity upon discontinuation of treatment. The analysis of PGE2 1evels in the callus suggests that the effects of these drugs may not simply be related to their actions on PGE2 1evels but that the specific COX2 effectS may be related to other phamacological actions that are not clearly defined. Extraplation of these findings to a clinical setting suggests that management of fracture-associated pain with inhibitors of COX-2 should neither impair nor delay healing as Iong as the duration of treatment is consistent with current standards of care