| 1. |
- Acosta, Stefan, et al.
(författare)
-
Epidemiology and Prognostic Factors in Acute Superior Mesenteric Artery Occlusion.
- 2010
-
Ingår i: Journal of Gastrointestinal Surgery. - : Springer Science and Business Media LLC. - 1873-4626 .- 1091-255X. ; 14, s. 628-635
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Reports on trends in incidence and mortality of acute superior mesenteric artery (SMA) occlusion and evaluation of prognostic factors in recent years are lacking. METHODS: Patients with acute SMA occlusion were identified through the in-patient and autopsy registry between 1970 and 1982 (n = 270), 1987 to 1996 (n = 135), and 2000 and 2006 (n = 100) in Malmö, Sweden. RESULTS: The overall incidence rate decreased from 8.6 to 5.4/100,000 person years and the autopsy rate from 87% to 25% over time. A higher serum creatinine level was associated with a lower probability of undergoing multi-detector row computed tomography with intravenous contrast (MDCTiv) (p = 0.006). Not performing a MDCTiv (odds ratio 4.0; 95% confidence interval [1.0-16.0]) remained as independent prognostic factor for in-hospital mortality. General and vascular surgeons collaborated in 25 out of 61 patients that underwent an intervention, of which 21 (84%) (p < 0.001) survived. CONCLUSIONS: A close collaboration between radiologists and general and vascular surgeons seems to be most important to lower the mortality in patients with acute SMA occlusion.
|
|
| 2. |
- Akesson, Oscar, et al.
(författare)
-
Morbidity related to defunctioning loop ileostomy in low anterior resection
- 2012
-
Ingår i: International Journal of Colorectal Disease. - : Springer Science and Business Media LLC. - 1432-1262 .- 0179-1958. ; 27:12, s. 1619-1623
-
Tidskriftsartikel (refereegranskat)abstract
- Aim A defunctioning loop ileostomy in low anterior resection reduces the incidence and morbidity of an anastomotic leakage, but complications related to the stoma may occur. We explored stoma-associated complications during the stoma period and after stoma reversal. Methods A retrospective analysis of rectal cancer patients operated with low anterior resection and a defunctioning loop ileostomy at Helsingborg Hospital and Malmo University Hospital from January 2007 to June 2009 was undertaken. Results Ninety-two patients were included, of whom 82 (89 %) underwent stoma reversal. The median stoma period was 6.2 +/- 3.2 months. Sixty-six percent of the patients suffered from minor or major stoma-associated morbidity. The complication rate was significantly related to the stoma time (p < 0.01). Twenty-nine percent (27/92) had at least one episode of dehydration, leading to readmittance in half of the cases. Elderly patients were more prone to develop dehydration. Dehydration most commonly occurred early in the postoperative period (mean, 5.8 weeks). The mean hospital stay for stoma reversal was 6.5 +/- 4.0 days. Forty percent (33/82) had some complication associated with the reversal. Conclusion This study indicates high morbidity associated with defunctioning loop ileostomy. Our data suggest that the stoma time should be limited to reduce complications. Monitoring and early stoma reversal should be considered in elderly patients. Furthermore, stoma reversal is not uneventful, and more studies are needed to address how to minimize complications.
|
|
| 3. |
|
|
| 4. |
- Awla, Darbaz, et al.
(författare)
-
Neutrophil-derived matrix metalloproteinase-9 is a potent activator of trypsinogen in acinar cells in acute pancreatitis.
- 2012
-
Ingår i: Journal of Leukocyte Biology. - : Oxford University Press (OUP). - 1938-3673 .- 0741-5400. ; 91, s. 711-719
-
Tidskriftsartikel (refereegranskat)abstract
- MMPs are generally considered to regulate degradation and remodeling of the ECM. Convincing data also implicate a role for MMPs in inflammatory conditions, such as AP, although the mechanisms are not known. The aim of this study was to define the role of MMPs in regulating activation of trypsinogen and tissue damage in AP, which was induced by infusion of taurocholate into the pancreatic duct in mice. A broad-spectrum MMP inhibitor (BB-94) and MMP-9 gene-deficient mice were used. Neutrophil secretions and rMMP-9 were used to stimulate trypsinogen activation in isolated acinar cells. Taurocholate challenge increased serum amylase, neutrophil infiltration, MIP-2 (CXCL2) formation, trypsinogen activation, and tissue damage in the pancreas. Treatment with the broad-spectrum inhibitor of MMPs, BB-94, markedly reduced activation of trypsinogen, levels of CXCL2, infiltration of neutrophils, and tissue damage in AP. Taurocholate challenge increased serum levels of MMP-9 but not MMP-2. Taurocholate-induced amylase levels, neutrophil accumulation, production of CXCL2, trypsinogen activation, and tissue damage in the pancreas were abolished in MMP-9-deficient mice. Moreover, secretions from activated neutrophils isolated from WT but not from MMP-9-deficient animals stimulated trypsinogen activation in acinar cells. Notably, rMMP-9 greatly enhanced activation of trypsinogen in acinar cells. These findings demonstrate that neutrophil-derived MMP-9 is a potent activator of trypsinogen in acinar cells and regulates pathological inflammation and tissue damage in AP.
|
|
| 5. |
- Bjursten, Henrik, et al.
(författare)
-
S100B Profiles and Cognitive Function at High Altitude
- 2010
-
Ingår i: High Altitude Medicine & Biology. - : Mary Ann Liebert Inc. - 1527-0297 .- 1557-8682. ; 11:1, s. 31-38
-
Tidskriftsartikel (refereegranskat)abstract
- Bjursten, Henrik, Per Ederoth, Engilbert Sigurdsson, Magnus Gottfredsson, Ingvar Syk, Orri Einarsson, and Tomas Gudbjartsson. S100B profiles and cognitive function at high altitude. High Alt. Med. Biol. 11:31-38, 2010.-Exposure to high altitude can lead to acute mountain sickness (AMS) and high altitude cerebral edema (HACE). In this study we investigated the effect of high altitude on neurocognitive function and S100B release. Increased S100B release has been hypothesized to signify a loss of integrity in the blood-brain barrier (BBB). Seven healthy volunteers trekked to Capanna Regina Margherita (4554 m above sea level) in the Monte Rosa massif. During ascent and descent, five test events were undertaken; participants underwent neurocognitive testing, Lake Louise scoring (LLS), and blood sampling to measure levels of S100B. The blood tests revealed that S100B levels increased 42% to 122% from baseline, and mean LLS increased from 0.57 to 2.57. A significant correlation was observed between both S100B levels and LLS and S100B and some neurocognitive scores. The study indicates that S100B can be released by a mild hypoxia during AMS. Moreover, an observed correlation between S100B and a lower score on neurocognitive tests suggests that the pathogenetic mechanisms may be linked. The study indicates that a decline in cognitive function is associated with symptoms of AMS.
|
|
| 6. |
- Buchwald, Pamela, et al.
(författare)
-
Standard protocol for assessment of colon cancer improves the quality of pathology.
- 2011
-
Ingår i: Colorectal Disease. - : Wiley. - 1462-8910. ; 13, s. 33-36
-
Tidskriftsartikel (refereegranskat)abstract
- Aim: Tumour stage is the most important prognostic factor in colon cancer. The aim of this study was to examine the impact on the quality of pathology by the use of a standardized PAD protocol. Method: A standardized PAD protocol for colorectal cancer was developed and all patients subjected to colon resection due to adenocarcinomas between 2004 and 2006 were analyzed concerning lymph node status, circumferential resection margin (CRM), intravascular and perineural growth. Moreover, usage of the PAD protocol and whether a pathologist or biomedicine analytic technician (BMA) performed the lymph node dissection was noted and also if the surgical procedure was elective or acute. Results: During the study period 302 colon resections were carried out. The standard protocol was employed in 68% of the cases varying from 0-100% between pathologists. The median number of investigated lymph nodes was 16 ± 11. When the lymph node dissection was performed by a BMA, significantly more lymph nodes were examined; 22 ± 15 and 14 ± 9 respectively (p<0.01). There was a positive correlation between application of the standard protocol and the number of analyzed lymph nodes (<0.05). Comments on CRM, perineural growth and intravascular growth were also significantly more frequent when the protocol was used. Emergency surgery did not influence the handling of the specimens. Conclusion: Minor efforts in terms of a standard protocol for pathology and specimen dissection by BMAs, leading to an increased quality of the PAD-report may also improve long term outcome for patients.
|
|
| 7. |
- Hasan, Zirak, et al.
(författare)
-
Geranylgeranyl transferase regulates CXC chemokine formation in alveolar macrophages and neutrophil recruitment in septic lung injury
- 2013
-
Ingår i: American Journal of Physiology: Lung Cellular and Molecular Physiology. - : American Physiological Society. - 1522-1504 .- 1040-0605. ; 304:4, s. 221-229
-
Tidskriftsartikel (refereegranskat)abstract
- Hasan Z, Rahman M, Palani K, Syk I, Jeppsson B, Thorlacius H. Geranylgeranyl transferase regulates CXC chemokine formation in alveolar macrophages and neutrophil recruitment in septic lung injury. Am J Physiol Lung Cell Mol Physiol 304: L221-L229, 2013. First published December 14, 2012; doi:10.1152/ajplung.00199.2012.-Overwhelming accumulation of neutrophils is a significant component in septic lung damage, although the signaling mechanisms behind neutrophil infiltration in the lung remain elusive. In the present study, we hypothesized that geranylgeranylation might regulate the inflammatory response in abdominal sepsis. Male C57BL/6 mice received the geranylgeranyl transferase inhibitor, GGTI-2133, before cecal ligation and puncture (CLP). Bronchoalveolar lavage fluid and lung tissue were harvested for analysis of neutrophil infiltration, as well as edema and CXC chemokine formation. Blood was collected for analysis of Mac-1 on neutrophils and CD40L on platelets. Gene expression of CXC chemokines, tumor necrosis factor-alpha (TNF-alpha), and CCL2 chemokine was determined by quantitative RT-PCR in isolated alveolar macrophages. Administration of GGTI-2133 markedly decreased CLP-induced infiltration of neutrophils, edema, and tissue injury in the lung. CLP triggered clear-cut upregulation of Mac-1 on neutrophils. Inhibition of geranylgeranyl transferase reduced CLP-evoked upregulation of Mac-1 on neutrophils in vivo but had no effect on chemokine-induced expression of Mac-1 on isolated neutrophils in vitro. Notably, GGTI-2133 abolished CLP-induced formation of CXC chemokines, TNF-alpha, and CCL2 in alveolar macrophages in the lung. Geranylgeranyl transferase inhibition had no effect on sepsis-induced platelet shedding of CD40L. In addition, inhibition of geranylgeranyl transferase markedly decreased CXC chemokine-triggered neutrophil chemotaxis in vitro. Taken together, our findings suggest that geranylgeranyl transferase is an important regulator of CXC chemokine production and neutrophil recruitment in the lung. We conclude that inhibition of geranylgeranyl transferase might be a potent way to attenuate acute lung injury in abdominal sepsis.
|
|
| 8. |
- Hasan, Zirak, et al.
(författare)
-
Rho-kinase regulates induction of T-cell immune dysfunction in abdominal sepsis.
- 2013
-
Ingår i: Infection and Immunity. - 1098-5522. ; 81:7, s. 2499-2506
-
Tidskriftsartikel (refereegranskat)abstract
- T-cell dysfunction increases susceptibility to infections in patients with sepsis. In the present study, we hypothesized that Rho-kinase signaling might regulate induction of T-cell dysfunction in abdominal sepsis. Male C57BL/6 mice were treated with the specific Rho-kinase inhibitor Y-27632 (5 mg/kg) prior to cecal ligation and puncture (CLP). Spleen CD4 T-cell apoptosis, proliferation and regulatory T-cells (CD4(+)CD25(+)Foxp3(+)) were determined by flow cytometry. Formation of IFN-γ and IL-4 in the spleen and plasma levels of HMBG1 and IL-6 were quantified by use of ELISA. It was found that CLP evoked apoptosis and decreased proliferation in splenic CD4 T-cells. Inhibition of Rho-kinase activity decreased apoptosis and enhanced proliferation of CD4 T-cells in septic animals. In addition, CLP-evoked induction of regulatory T-cells in the spleen was abolished by Rho-kinase inhibition. CLP reduced the levels of IFN-γ and IL-4 in the spleen. Pretreatment with Y-27632 inhibited the sepsis-induced decrease in IFN-γ but not IL-4 formation in the spleen. CLP increased plasma levels of HMGB1 by 20-fold and IL-6 by 19-fold. Inhibition of Rho-kinase decreased this CLP-evoked increase of HMGB1, IL-6 and IL-17 levels in the plasma by more than 60%, suggesting that Rho-kinase regulates systemic inflammation in sepsis. Moreover, we observed that pretreatment with Y-27632 abolished CLP-induced bacteremia. Together, our novel findings indicate that Rho-kinase is a powerful regulator of T-cell immune dysfunction in abdominal sepsis. Thus, targeting Rho-kinase signaling might be a useful strategy to improve T-cell immunity in patients with abdominal sepsis.
|
|
| 9. |
- Hasan, Zirak, et al.
(författare)
-
Rho-Kinase Signaling Regulates Pulmonary Infiltration of Neutrophils in Abdominal Sepsis via Attenuation of CXC Chemokine Formation and Mac-1 Expression on Neutrophils.
- 2012
-
Ingår i: Shock. - 1540-0514. ; 37:3, s. 282-288
-
Tidskriftsartikel (refereegranskat)abstract
- ABSTRACT: Excessive neutrophil infiltration is a major component in septic lung injury, although the signaling mechanisms behind pulmonary recruitment of neutrophils in polymicrobial sepsis remain elusive. Herein, we hypothesized that Rho-kinase activity may play a significant role in pulmonary neutrophil recruitment and tissue damage in abdominal sepsis. Male C57BL/6 mice were treated with the Rho-kinase inhibitor Y-27632 (0.5 or 5 mg/kg) before cecal ligation and puncture. Bronchoalveolar lavage fluid and lung tissue were harvested for analysis of neutrophil infiltration, as well as edema and CXC chemokine formation. Blood was collected for analysis of Mac-1 on neutrophils and CD40L on platelets as well as soluble CD40L and metalloproteinase-9 (MMP-9) in plasma. CLP triggered significant pulmonary damage characterized by neutrophil infiltration, increased levels of CXC chemokines, and edema formation in the lung. Furthermore, CLP up-regulated Mac-1 expression on neutrophils, decreased CD40L on platelets and increased soluble CD40L and MMP-9 in the circulation. Interestingly, inhibition of Rho-kinase dose-dependently decreased CLP-induced neutrophil expression of Mac-1, formation of CXC chemokines and edema as well as neutrophil infiltration and tissue damage in the lung. Moreover, Rho-kinase inhibition significantly reduced sepsis-provoked gene-expression of CXC chemokines in alveolar macrophages. In contrast, Rho-kinase inhibition had no effect on platelet shedding of CD40L or plasma levels of MMP-9 in septic mice. In conclusion, these data demonstrate that the Rho-kinase signaling pathway plays a key role in regulating pulmonary infiltration of neutrophils and tissue injury via regulation of CXC chemokine production in the lung and Mac-1 expression on neutrophils in abdominal sepsis.
|
|
| 10. |
- Hwaiz, Rundk, et al.
(författare)
-
Rac1 signaling regulates sepsis-induced pathologic inflammation in the lung via attenuation of Mac-1 expression and CXC chemokine formation.
- 2013
-
Ingår i: Journal of Surgical Research. - : Elsevier BV. - 1095-8673 .- 0022-4804. ; 183:2, s. 798-807
-
Tidskriftsartikel (refereegranskat)abstract
- Excessive neutrophil recruitment is a major feature in septic lung damage although the signaling mechanisms behind pulmonary infiltration of neutrophils in sepsis remain elusive. In the present study, we hypothesized that Rac1 might play an important role in pulmonary neutrophil accumulation and tissue injury in abdominal sepsis. Male C57BL/6 mice were treated with Rac1 inhibitor NSC23766 (5 mg/kg) before cecal ligation and puncture (CLP). Bronchoalveolar lavage fluid and lung tissue were collected for the quantification of neutrophil recruitment and edema and CXC chemokine formation. Blood was collected for the determination of Mac-1 on neutrophils and proinflammatory compounds in plasma. Gene expression of CXC chemokines and tumor necrosis factor alpha was determined by quantitative reverse transcription-polymerase chain reaction in alveolar macrophages. Rac1 activity was increased in lungs from septic animals, and NSC23766 significantly decreased pulmonary activity of Rac1 induced by CLP. Administration of NSC23766 markedly reduced CLP-triggered neutrophil infiltration, edema formation, and tissue damage in the lung. Inhibition of Rac1 decreased CLP-induced neutrophil expression of Mac-1 and pulmonary formation of CXC chemokines. Moreover, NSC23766 abolished the sepsis-evoked elevation of messenger RNA levels of CXC chemokines and tumor necrosis factor alpha in alveolar macrophages. Rac1 inhibition decreased the CLP-induced increase in plasma levels of high mobility group protein B1 and interleukin 6, indicating a role of Rac1 in systemic inflammation. In conclusion, our results demonstrate that Rac1 signaling plays a key role in regulating pulmonary infiltration of neutrophils and tissue injury via regulation of chemokine production in the lung and Mac-1 expression on neutrophils in abdominal sepsis. Thus, targeting Rac1 activity might be a useful strategy to protect the lung in abdominal sepsis.
|
|
