The Pararectus approach provides secure access to the deep circumflex iliac vessel for harvest of a large sized and vascularized segment of the iliac crest.

BACKGROUND: The feasibility of harvesting a vascularized iliac crest utilizing the Pararectus approach was assessed in cadavers and then this new technique was implemented in a clinical case. METHODS: Bilaterally in five cadavers the branches of both external iliac arteries were injected with colored silicone to assess their position to each other and to harvest a bone graft vascularized by the deep circumflex iliac artery (DCIA) through the Pararectus approach. This technique was implemented in a 68-years-old female patient, initially admitted to a level-I-trauma center after sustaining multiple injuries by falling from great height. For definitive treatment of a severely contaminated medially open (Gustilo-Anderson Type 3A) calcaneal luxation fracture (Sanders type IIIBC) in this patient a vascularized iliac crest autograft harvest by the Pararectus approach was used for reconstructive surgery. RESULTS: The DCIA and the deep inferior epigastric vessels (DIEV: vascularizing the rectus abdominis muscle and main pedicle of the inferiorly based rectus abdominis myocutaneous flap) are very close on the lateral and medial border of the external iliac artery, respectively. As a consequence, the retrograde dissection of the DIEV towards the DCIA through the Pararectus approach made the dissection of the vascularized iliac crest more amenable, preserving both the lateral femoral cutaneous and the genitofemoral nerves. Four months after the surgery the patient was able to fully weight-bear in orthopedic shoes. Radiographs and CT scans showed correct hind foot alignment and bony integration of the vascularized iliac crest graft into the residual calcaneal body. CONCLUSION: The Pararectus approach allowed for secure collection of large vascularized iliac grafts. The presented technique was successful as a salvage procedure in a clinical case with substantial bone loss after an open calcaneal fracture.

Aetiology of adult burns treated from 2000 to 2012 in a Swiss University Hospital.

BACKGROUND: Burns in Switzerland are frequent and lead to high economic and social costs. However, little is known about the aetiology of burns suffered by patients seeking treatment in hospital emergency departments. This knowledge could be used to develop preventive measures. METHODS: This retrospective analysis included all patients (≥16 years old) with acute thermal injuries of known cause admitted to the adult emergency department in Bern University Hospital (Switzerland, not a specialised burns unit) between 2000 and 2012. Clinical and sociodemographic data were extracted from medical records, i.e. the environment in which the burn occurred, as well as details of burn severity and aetiology. RESULTS: Seven hundred and one (701) patients with a mean age of 35.0±14.5 years (56% men) were included in the analysis. The winter season and the days around Christmas, turn of the year and Swiss National Day were identified as times with high risk of burns. Household (45%) and workplace (31%) were the most common locations/settings in which the burns occurred. Approximately every second burn was caused by scald, every fourth by flame and every seventh by hot objects. The analysis identified cooking, tar and electricity in workplace accidents, barbecues and the use of gasoline as aetiological factors in burns in leisure time, together with water in domestic thermal injuries. Burns occurred predominantly on non-protected skin on the hand and arms. The most severe burns were seen in electrical and flame burns. Men suffered more severe burns than women in all settings except psychopathology. CONCLUSIONS: The data suggest that the incidence and severity of burns in Switzerland could be reduced by preventive strategies and public campaigns, including education on fire protection systems, raising awareness about the times and locations where the risks of burns are greater, further improvement in workplace safety, particularly with cooking facilities and electrical equipment, and the development of innovative safety devices (i.e. machines, protective gloves). These findings have to be interpreted carefully, as this study includes only adult patients who presented in our ED and, in most cases, the burns covered less than 20% of the body surface.

FT-IR product study of the reactions of NO3 radicals with ortho-, meta-, and para-cresol.

Product analyses of the NO3 radical-initiated oxidation of ortho-, meta-, and para-cresol have been performed in large-volume chamber systems at the University of Wuppertal (1080 L quartz glass reactor: QUAREC) and the European Photoreactor (EUPHORE), Valencia, Spain. The reaction of O3 with NO2 was used for the in situ generation of NO3 radicals in both QUAREC and EUPHORE. In the QUAREC experiments the gas-phase reaction of ortho-cresol isomer with NO3 yielded (11.5 ± 0.8) % 6-methyl-2-nitrophenol (6M2NP), (4.4 ± 0.3) % methyl-1,4-benzoquinone (MQUIN) and (77.2 ± 6.3) % HNO3. The reaction of NO3 radicals with meta-cresol yielded (21.2 ± 1.4) % 3-methyl-2-nitrophenol (3M2NP), (22.8 ± 1.8) % 3-methyl-4-nitrophenol (3M4NP), (23.5 ± 1.8) % 5-methyl-2-nitrophenol (5M2NP), (4.2 ± 0.7) % MQUIN and (72.3 ± 6.4) % HNO3. In the reaction of NO3 radicals with para-cresol, 4-methyl-2-nitrophenol (4M2NP) and HNO3 were identified as products with yields of (41.3 ± 3.7) % and (85.0 ± 10.2) %, respectively. In the EUPHORE chamber not all products were formed at levels above the detection limit, however, in cases where detection was possible similar product yields were observed. The product formation yields determined in both chambers are compared with available literature data and a gas-phase mechanism is proposed to explain the formation of the products observed from the reaction of NO3 and with cresol isomers.

Serum trace metal and ceruloplasmin variability in individuals treated for pulmonary tuberculosis.

SETTING: Investigation of trace metal behaviour during the treatment of active pulmonary tuberculosis (PTB) patients residing in Romania. OBJECTIVE: To assess, follow and identify serum iron (Fe), copper (Cu) and zinc (Zn) levels in patients diagnosed and treated for active PTB. DESIGN: Chemical and statistical analysis of various biochemical parameters in 47 subjects diagnosed with active PTB and 170 healthy Romanian residents. RESULTS: Copper and ceruloplasmin levels were increased in patients with active PTB compared to the control group (P < 0.01), while the serum Zn level was significantly lower than in healthy subjects (P < 0.01) or within the normal range. The present study shows that there is a significant correlation between serum Cu concentrations and ceruloplasmin. CONCLUSIONS: This study provides preliminary evidence that Zn and Fe redistribution is operating as a primary host defence mechanism to reduce the availability of metals for microbial metabolism during infection. The study also calls attention to the fact that anti-tuberculosis treatment is sufficient to enhance the concentration of the antioxidant species (Cu and ceruloplasmin). The data obtained suggest that serum Cu, Zn and Cu/Zn levels may serve as indirect pointers in the diagnosis of a disease but they cannot be considered as specific markers for TB.

The homologous and interspecies transmission of Cryptosporidium parvum and Cryptosporidium meleagridis.

Experimental infections have been performed in several mammals and birds to determine the host's specificity for Cryptosporidium parvum (of human and bovine origin) and for Cryptosporidium meleagridis (isolated from broiler chicken). The C. parvum infection (of human origin) was established also in calves (Bos taurus), lambs (Ovis aries), mice (Mus musculus), and rats (Ratus norvegicus), but not in broiler chickens (Gallus domestica). The C. parvum infection (of bovine origin), was achieved in calves, lambs, dogs (Canis familiaris), cats (Felis domesticus), rabbits (Orytolagus cuniculus), mice, rats, and guinea-pigs (Cavia porcelus) but not in broiler chickens. We have demonstrated that C. meleagridis can produce infection in broiler chickens and in 5 mammalian species (calves, pigs, rabbits, rats, mice) but not in guinea-pigs.

Alveolar macrophage release of tumor necrosis factor-alpha in chronic alcoholics without liver disease.

Alcohol is an immunosuppressive drug, and chronic abuse has been associated with increased susceptibility to a variety of infections, including bacterial pneumonia and tuberculosis. Alveolar macrophages are the resident phagocytes of the lung and play a central role in lung host defenses against infection ranging from direct antibacterial activity to the release of proinflammatory cytokines such as tumor necrosis factor-alpha (TNFalpha). TNFalpha, in particular, plays a key role in the development of the early inflammatory response. In this study, we investigated the effects of chronic alcohol consumption on alveolar macrophage release of TNFalpha in vitro. We prospectively studied lipopolysaccharide (LPS)-stimulated release of TNFalpha from alveolar macrophages obtained from bronchoalveolar lavage fluid (BALF) in 22 alcoholic (18 smokers, 4 nonsmokers) and 7 nondrinking healthy volunteers (3 smokers, 4 nonsmokers). The total number of cells recovered by bronchoalveolar lavage (BAL) and their differential distribution were not significantly different in alcoholics versus controls (43 +/- 8 x 10(6) and 39 +/- 13 x 10(6), respectively). However, the total number of cells recovered from BALF was significantly higher in smokers (51 +/- 8 x 10(6)) than in nonsmokers (19 +/- 5 x 10(6)). Spontaneous (basal) release of TNFalpha by alveolar macrophages was the same in alcoholics and controls. In contrast, LPS-stimulated release of TNFalpha was significantly suppressed in alcoholics compared with that of controls (1343 +/- 271 vs. 3806 +/- 926 U TNF/ml/10(6) cells, respectively, p < 0.015). When controlled for smoking, LPS-stimulated TNFalpha production was suppressed in alcoholic nonsmokers (563 +/- 413 U TNF/ml/10(6)) compared with control nonsmokers (5113 +/- 1264 U TNF/ml/10(6)). LPS-stimulated TNFalpha production was also less in control smokers (2063 +/- 386 U TNF/ml/10(6) cells) than in control nonsmokers (5113 +/- 1264 U TNF/ml/10(6) cells). There was no difference in TNFalpha production between smoking alcoholics and smoking control subjects. We conclude that chronic alcohol consumption significantly suppresses LPS-stimulated alveolar macrophage production of TNFalpha. This effect is obscured if the subject also smokes. Because TNFalpha production is an important element in host defense, this may explain, in part, the susceptibility of chronic alcohol abusers to a variety of infections.

Alcohol decreases T-lymphocyte migration into lung tissue in response to Pneumocystis carinii and depletes T-lymphocyte numbers in the spleens of mice.

Previous work from our laboratory has shown that chronic alcohol consumption in mice creates immunosuppression sufficient to permit infection with the opportunistic pathogen Pneumocystis carinii. Host defense against P. carinii is critically dependent upon host T lymphocytes. In these experiments, we address the effect of chronic alcohol consumption on recruitment of T lymphocytes into infected lung tissue and on lymphocytes in host lymphoid tissue. We find that mice administered alcohol in drinking water and then inoculated with P. carinii show significantly decreased recruitment of CD4+ and CD8+ T lymphocytes into lung tissue in comparison with control mice. Additional experiments show significant depletion of CD4+ lymphocytes in spleens from alcohol mice and decreased numbers of activated T lymphocytes. Analysis of surface expression of the adhesion molecules LFA-1, VLA-4, and ICAM-1 show no significant differences in lymphocytes from alcohol-consuming mice, and lymphocyte chemotaxis in vitro is also unaltered. We conclude that chronic consumption of alcohol impairs lung recruitment of lymphocytes in response to an infectious challenge. This impaired lymphocyte recruitment may be a consequence of depletion of T lymphocytes in host lymphoid tissue. Impaired recruitment of lymphocytes may explain the increased morbidity and mortality of pulmonary infections in alcoholic subjects.

Aspects of hydatidosis in the adult population in Banat.

An epidemiological study was performed on a lot of 505 adult subjects (over 20 years old) diagnosed with E.granulosus hydatidosis and operated in surgery units in hospitals from such towns as Timisoara, Arad and Resita (1985-1992). The incidence of hydatid infection was almost uniformly distributed by sexes, being a little higher in rural areas (52.0%); the highest number of cases was reported in Timis County (63.6%), followed by Caras-Severin County (21.2%). Hydatidosis was most frequently found in liver (67.5%) and lungs (23.7%) and more rarely in kidneys (0.4%), brain (0.2%), pancreas (0.2%), ovary (0.2%). Secondary hydatidosis was reported on 12.7% of cases and multiple cyst forms in 12.7% of cases. The distribution of cases by age group was relatively balanced, a slightly increased incidence being found in the 20-29 years age group (23.2%), about 1/3 of pulmonary localizations being reported in the age group. Post-surgery complications were reported in 13.5% of the total hepatic localizations and in 30% of the pulmonary localizations. The average number of days in hospital was 29.5 days/case. The average morbidity in the adult population in Banat over an eight years time interval was 5.36%ooo, being higher in Timis county-7.8%ooo where a peak (11%ooo) was reported in 1987.

Nitric oxide and host defense against Pneumocystis carinii infection in a mouse model.

To investigate whether successful host defense against Pneumocystis carinii is dependent on induction of inducible nitric oxide synthase (iNOS) in alveolar macrophages, immunocompetent mice, mice depleted of CD4 lymphocytes with anti-CD4 antibody, and mice with severe combined immunodeficiency (scid) were inoculated intratracheally with P. carinii. Three weeks later, immunocompetent mice had cleared the organisms completely, while CD4 cell-depleted and scid mice were severely infected (scores, 3.6 +/- 0.2 and 2.8 +/- 0.2, respectively). Inflammation scores were significantly higher in CD4 cell-depleted mice (3.4 +/- 0.2) than in scid mice (0.6 +/- 0.2). Minimal iNOS mRNA was detectable in lung tissue from immunocompetent mice; iNOS mRNA was comparable in scid mice and mice inoculated with PBS but was 6-fold higher in CD4 cell-depleted mice. Immunohistochemistry localized iNOS protein to alveolar macrophages in CD4 cell-depleted mice. Thus, iNOS is an unlikely participant in host defense against P. carinii, because enzyme expression does not correlate with either clearance or severity of infection.