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Acute phase response in infectious disease.

In considering the pathology associated with infectious diseases, the most common host response to such infection is inflammation. The mechanism(s) whereby inflammation is initiated and the cell types involved will dictate the kinds of acute phase plasma changes that can be seen associated with the infection. Bacteria seem to initiate the classical type of inflammatory response and plasma protein changes similar to those seen in experimental inflammation induced by chemical means. Viruses, on the other hand, in the absence of cytopathology do not appear to induce the same kind of inflammatory changes and avoid the induction of the acute phase protein response since they may not initiate activation of monocytes and/or macrophages. Those viruses that do cause macrophage activation would be expected to have acute phase protein changes associated with that activation. Parasites, however, appear to initiate the acute phase plasma response only when their migration leads to tissue destruction and local inflammation such as caused by parasitemia with Trypanosoma cruzi in the mouse or with migration of Nippostrongylus brasiliensis in the rodent. Human parasitic diseases require much more investigation in order to clarify the role played by acute phase proteins in the subsequent establishment of the host-parasite relationship. We postulate that the macrophage or monocyte on interaction with the infectious pathogen becomes activated and secretes a number of factors, including interleukin 1 and hepatocyte-stimulating factor, which have a marked effect on the total acute phase reaction. In addition to an effect on phagocytic and immune systems, the mediators cause hepatocytes to markedly increase the secretion of plasma acute phase proteins. Some of these proteins return to the site of inflammation and interact with the infectious pathogen and/or cells and proteins of the host, thereby affecting the final outcome of inflammation. We also propose that the initial interaction of an organism such as a parasite and the mammalian host involves early recognition by the macrophage, thereby initiating both the humoral and cellular acute phase reactions and subsequently affects the immune response against the parasite. Variations in the acute phase reaction may help to explain differences in susceptibility to infectious organisms and the presence or lack of host killing mechanisms for the parasite.

Acute-Phase Proteins↗

The effect of increased intracranial pressure (ICP) on gastric motility.

This study evaluates the effect of increased intracranial pressure (ICP) on gastric motility. Nine male cats (weight, 4.84 +/- 1.16 kg) were anesthetized with ketamine and underwent laparotomy for placement of bipolar (silver-silver chloride) electrodes on the serosal surface of the gastroesophageal junction (GEJ), antrum, and prepyloric areas of the stomach. At 1 week frontoparietal burr holes were performed with placement of an epidural Fogarty catheter. Migrating myoelectric complexes (MMCs) were evaluated at the GEJ, antrum, and prepyloric areas at varying levels of ICP (baseline and 20, 40, and 60 mm Hg) using balloon inflation. MMCs at the GEJ were triphasic with a period of 4 sec (+/- 1 sec) at baseline levels. At ICP levels above baseline, periodicity and waveforms at the GEJ became irregular. Waveforms became multiphasic with 1- to 2-sec periods and variable amplitudes. In the antral and prepyloric areas, duration and amplitude of the triphasic MMCs was unchanged from baseline. At 60 mm Hg ICP periodicity was significantly altered at both 1 and 2 weeks. MMCs returned to baseline levels with balloon deflation. The data indicate that elevated ICP (to 60 mm Hg) results in consistent and reproducible alterations of MMC periodicity, suggesting that such alterations may influence gastric motility.

Animals↗

A pilot study of magnetic resonance imaging-guided closed reduction of cervical spine fractures.

STUDY DESIGN: We report on a prospective selective case series of 17 patients with cervical fracture-dislocations treated with closed reduction under MRI guidance. OBJECTIVE: To demonstrate the safe and effective use of in-line axial traction in the reduction of cervical fracture-dislocations using MRI guidance. SUMMARY OF BACKGROUND DATA: Closed reduction of the cervical spine for acute fracture-dislocations has been a traditional technique used for restoring vertebral alignment and providing neural element decompression. The safety of this technique has been questioned, with concerns of disc migration and overdistraction causing neurologic worsening cited as reasons to choose operative reduction and decompression as a safer option in some circumstances. METHODS: Seventeen patients with fracture-dislocations of the subaxial cervical spine were given a trial of traction under MRI guidance between 1999 and 2003. The incidence of posteriorly herniated disc material was noted, and the diameter of the spinal canal at the injured level was recorded before and after traction. RESULTS: All patients tolerated traction without neurologic worsening. Pretraction disc disruption was found in 15 of 17 (88.2%) of patients, with posterior herniation in 4 of 17 (23.5\%). Traction caused a return of herniated disc material toward the disc space in all cases. Canal dimensions improved in 11 of 17 patients, with canal diameter increasing by a factor of 1.1 to 3.0, with a mean improvement of 1.73. The process of reduction was observed to be a gradual one, with progressive, significant improvement in canal dimensions occurring before anatomic realignment. As distracting force was increased, sequential MRIs showed that canal dimensions did not diminish at any time in any patient. CONCLUSIONS: MRI monitoring in closed cervical reduction is a useful research tool for this technique. Closed reduction appears to be safe as used in this preliminary study and is effective in achieving immediate spinal cord decompression.

Adult↗

Neointimal Hyperplasia in Coronary Vein Grafts: Pathophysiology and Prevention of a Significant Clinical Problem.

Abstract Neointimal hyperplasia in aortocoronary vein grafts represents a significant problem that, by itself or by development of vein graft atherosclerosis, leads to the return of symptoms and to major adverse cardiac events after coronary artery bypass grafting. The main causes of neointimal hyperplasia are surgical trauma, intraoperative ischemia reperfusion injury, and implantation of a vein into the arterial circulation. All these pathogenetic factors cause a loss of protective endothelial mediators. The initiating steps lead to the induction of a significant inflammatory response and to the production of mitogenic factors in the vascular wall. DNA synthesis in vascular smooth muscle cells is markedly up-regulated, and intracellular signal transduction leads to transcription of immediate early genes, which causes an intense proliferative response. Vascular smooth muscle cells proliferate, migrate through the internal elastic lamina with the support of proteases, and transform from contractile-type into secretory-type cells. A thick layer of neointima is formed. The prevention of neointimal hyperplasia includes meticulous surgical technique, the choice of a large target vessel, and adequate intraoperative storage of the vein graft. Local intraoperative therapy of the implanted graft has been successfully tested in the experimental setting with a variety of substances that tackle different steps in the pathologic mechanism. Systemic pharmacologic therapy in clinical use primarily consists of the use of platelet inhibitors and anticoagulants. The transfer of experimental knowledge to bedside application has been slow. Gene therapy represents a promising field for the improved management of vein graft neointimal hyperplasia.

Journal Article↗

Cyclic motor activity and trophicity after jejunal resection and bypass in rats.

The aim of the study was to examine the changes in intestinal motility induced by an extensive jejunal resection and bypass in rats using an electromyographic technique. The relationship, if any, between the development of motility and adaptive modifications of intestinal trophicity was also studied. A massive jejunal resection, preserving a 7-cm segment distal to the ligament of Treitz, was performed in one group of animals. In a second group, the jejunum was bypassed as a self-emptying blind loop. Two sham-operated groups underwent transection and reanastomosis on the proximal jejunum or ileum. Electromyographic activity was studied at the 10th and 30th postoperative days by means of electrodes implanted throughout the remaining or bypassed bowel and was expressed by means of the pattern of recurrence of the migrating myoelectric complex (MMC). After a month, the animals were sacrificed. Mucosal and muscular wet weight and protein content (mg/cm) of the intestine were then determined. The results showed that 10 days after the jejunal resection in the fasting state, MMC cycle duration is different in the remaining jejunum and in the ileum. However, the distribution of MMC phases in the jejunum was modified and was similar to the one in the ileum. Thirty days after resection, MMC cycle duration, as well as phase distribution in the remaining jejunum, resemble the MMC patterns in the ileum. These changes were not observed after bypass. After the return of MMCs after postprandial inhibition produced by a meal, MMC duration in the ileum was greatly decreased until a month after jejunal resection. In contrast, the jejunal bypass did not produce this modification.

Action Potentials↗

Differential effects of ischemia and reperfusion on c-Jun N-terminal kinase isoform protein and activity.

Activation of the c-Jun N-terminal (JNK) or stress-activated protein kinases (SAPK) is associated with a wide range of disparate cellular responses to extracellular stimuli, including either induction of or protection from apoptosis. This study investigates the effect of ischemia and reperfusion on JNK isoform activities using a reversible rabbit spinal cord ischemia model. High basal JNK activity, attributed to the p46 JNK1 isoform, was expressed in the CNS of untreated rabbits. JNK activity decreased in the lumbar spinal cord of rabbits occluded for 15-60 min. During reperfusion animals occluded for 15 min recovered neurological function and JNK activity returned to normal levels. In contrast animals occluded for 60 min remained permanently paraplegic and JNK activity was half the control activity after 18 h of reperfusion. In these animals proteolytic fragments of JNK1 and JNK3 were observed and protein levels, but not activity, of JNK isoforms increased in a detergent-insoluble fraction. Two novel c-Jun (and ATF-2) kinase activities increased during reperfusion of animals occluded for 60 min. An activity designated p46(slow) was similar in M(r) to a JNK2 isoform induced in these animals. A second 30-kDa activity associated with the detergent-insoluble fraction co-migrated with a JNK3 N-terminal fragment. The results show that JNK1 is active in the normal CNS and increased activity is not associated with durations of ischemia and reperfusion that induce cell death. However, specific JNK isoform activation may participate in the cell death pathways as increased activity of novel c-Jun (ATF-2) kinase activities was observed in paraplegic animals.

Animals↗

Apolipoprotein J/clusterin is induced in vascular smooth muscle cells after vascular injury.

BACKGROUND: Understanding the precise molecular mechanisms underlying the phenomenon of restenosis after PTCA may help us to develop a new strategy for the treatment of restenosis after PTCA. The purpose of this study was to identify the genes involved in vascular restenosis. METHODS AND RESULTS: Applying a differential hybridization method to a model of the balloon-injured rabbit aorta, we identified 6 cDNA clones that were upregulated after injury. Northern blot showed that 5 genes, but not apolipoprotein J (apoJ)/clusterin, were constitutively expressed in noninjured aorta and upregulated after balloon injury. ApoJ mRNA was not detectable in noninjured aorta (control), began to be expressed at 6 hours after injury, showed a peak level at 24 hours (a 48-fold increase), gradually declined, and returned to the control level at 24 weeks. Western blot and immunohistochemistry demonstrated no expression of apoJ protein in noninjured aorta, an expression of apoJ at 2 days after balloon injury, and a peak level (a 55-fold increase) at 2 to 8 weeks. The expression of apoJ protein continued until 24 weeks after injury. In situ hybridization revealed that apoJ mRNA was expressed in smooth muscle cells (SMCs) of media at 2 days after injury and in SMCs of media and neointima at 2 weeks. To analyze the function of apoJ, stably transfected rabbit SMCs were created. The expression of apoJ stimulated proliferation and migration of SMCs. CONCLUSIONS: ApoJ is dramatically induced in media and neointima after vascular injury, suggesting that apoJ contributes to restenosis after angioplasty.

Angioplasty, Balloon, Coronary↗

[Immunological reactivity and the prognosis for allergic complications in the crew of the 2d Saliut-4 expedition].

Immunological reactivity of P. I. Klimuk and V. I. Sevastyanov was studied before and after their 63-day flight aboard the orbital station Salyut-4. The study used the methods to assay reactivity of T- and B-lymphocytes (PHA-blast-transformation, nonspecific formation of rosettes with sheep red blood cells, immunofluorescence to identify cells carrying immunoglobulin receptors on their surface, serum level of immunoglobulins as a function of Becells). Sensitization of the human body to allergenes of representatives of normal automicroflora of Staphylococcus, Streptococcus, Proteus and E. coli was examined. Specific immunological reactivity which was marked on the 2nd day and tended to return to normal on the 7th day postflight as well as a significant decrease of IgA were noted. Postflight P. I. Klimuk showed sensitization to allergens of Staphylococcus and Streptococcus. Results of immunological examinations of the first and second expeditions aboard the orbital station Salyut-4 were compared.

Adult↗

Entorhinal deafferentation induces the expression of profilin mRNA in the reactive microglial cells in the hippocampus.

Profilin has been identified as an actin monomer sequestering protein and is thought to be a key regulator of actin polymerization in many fundamental cellular processes. We report the expression of profilin mRNA in the murine hippocampus following transections of the entorhinal afferents. Northern blot analysis showed that transcript of profilin was upregulated in a transient manner in the deafferented rat hippocampus by 1.5-, 1.9-, 1.4-, and 1.1-fold of controls, respectively, at 1, 3, 7, and 15 days post-lesion. In situ hybridization confirmed the temporal upregulation of profilin mRNA in the deafferented zones of the mouse hippocampus, which showed a remarkable increase as early as at 1 day post-lesion, reached maximal level at 3 days post-lesion, and returned to the control level at 15 days post-lesion. The expression modulation of profilin mRNA was observed to occur specifically in the entorhinally denervated zones: the stratum lacunosum-moleculare of the hippocampus and the outer molecular layer of the dentate gyrus. The combination of in situ hybridization for profilin mRNA with lectin cytochemistry for Griffonia simplicifolia IB4 showed that the cells expressing profilin transcript in the denervated zones are activated microglial cells. The results suggest that the spatial and temporal upregulation of profilin mRNA in the hippocampus is induced by entorhinal deafferentation and profilin is involved in microglial activation associated with morphological change, migration, and phagocytic behavior of microglial cells.

Animals↗

[Prolonged peridural analgesia (PDA) for postoperative pain therapy after major urologic interventions. Experiences with 172 adult patients].

UNLABELLED: The benefits of epidural analgesia are well known, but it is not well understood which types of urologic surgery benefit most from epidural analgesia. In this study, the effects and side effects of prolonged epidural analgesia are prospectively examined and analysed on 172 adult patients in three different operation groups. An epidural infusion of local anaesthetic combined with an opioid and adrenaline was given for a period of 5-7 days. There was no difference between the groups with respect to the effectiveness of the analgesia and patients' perception of the treatment. Mobilization differed, as expected, between the groups, however even after the most major surgery (e. g. cystectomy with bladder substitution), mobilization was impressively unproblematic. Retarded return of regular intestinal function after the transperitoneal operation and partly after lumbotomy compared with the extraperitoneal operation depended on which operation was performed and the amount of analgesia given. The side effects such as sedation, nausea and pruritus were conditional partly on the opiate and partly on the intervention. Up to 11 % showed slight muscular weakness of the lower limbs as a specific side effect of the local anaesthetic. COMPLICATIONS: One patient died of cerebral hypoxia due to an initially undetected subdural catheter placement complicated by severe pre-existent carotid stenosis. In four patients, the epidural analgesia had to be stopped because of catheter migration. There was no clinical evidence of hematoma, abscess or permanent neurological damage. Epidural analgesia works well in terms of analgesia, mobilization and patient satisfaction, bearing in mind the potential side effects and complications. It can be recommended for lumbotomy and long transperitoneal operations however not for extraperitoneal interventions in the lower abdomen such as radical prostatectomy.

Adult↗

Immunoglobulin switch transcript production in vivo related to the site and time of antigen-specific B cell activation.

Immunoglobulin (Ig) class switch recombination is associated with the production and splicing of germline IgCH messenger RNA transcripts. Levels of gamma 1 transcripts in mouse spleen sections were assessed by semiquantitative analysis of reverse transcriptase polymerase chain reaction (PCR) products during primary and secondary antibody responses to chicken gamma globulin (CGG). This was correlated with the appearance of CGG-specific B cells and their growth and differentiation to plasma cells. After primary immunization with CGG, gamma 1 switch transcripts appeared after 4 d, peaked at a median of six times starting levels between 10 and 18 d after immunization, and returned to background levels before secondary immunization at 5 wk. By contrast, after secondary challenge with CGG, a sevenfold increase in transcripts occurs during the first d. The level again doubles by day 3, when it is six times that which is seen at the peak of the primary response. After day 4, there was a gradual decline over the next 2-3 wk. Within 12 h of secondary immunization, antigen-specific memory B cells appeared in the outer I zone and by 24 h entered S phase, presumably as a result of cognate interaction with primed T cells. Over the next few hours, they migrated to the edge of the red pulp, where they grew exponentially until the fourth day, when they synchronously differentiated to become plasma cells. The same pattern was seen for the migration, growth, and differentiation of virgin hapten-specific B cells when CGG-primed mice were challenged with hapten protein. The continued production of transcripts after day 3 indicates that switching also occurs in germinal centers, but in a relatively small proportion of their B cells. The impressive early production of switch transcripts during T cell-dependent antibody responses occurs in cells that are about to undergo massive clonal expansion. It is argued that Ig class switching at this time, which is associated with cognate T cell-B cell interaction in the T zone, has a major impact on the class and subclasses of Ig produced during the response.

Animals↗

Autoradiographic study of corneal neovascularization induced by chemical cautery.

The corneas of adult rats were cauterized chemically, and the responses of the pericorneal blood vessels and the cellular constituents of the cornea were followed by light microscopic autoradiography after labeling with 3H-thymidine. As in previous experiments, this injury elicited a neovascularization as capillaries sprouted and extended centripetally from the corneoscleral limbus to the cautery site. Chemical cautery induced a response in the epithelium, endothelium, and fibroblasts of the cornea as well as in the vascular cells. Elevated labeling indices for the corneal epithelium and endothelium began at 18 and 21 hours after injury, respectively. In all of these corneal cell types, the labeling index returned to control values by 75 hours. The onset and decline of DNA synthesis in corneal fibroblasts paralleled that of the corneal epithelium and endothelium. Labeling indices of vascular cells (endothelial cells and pericytes) increased 21 hours after injury, reached a maximal level at 45 hours, and returned to control values by 1 month after cautery. The first mitoses in vascular endothelial cells and pericytes were noted 36 hours after injury, and the initial capillary sprouts appeared at 39 hours. This study demonstrates that the thymidine incorporation by cells in the pericorneal blood vessels occurs early within the postcauterization period, at least 15 hours before the first mitotic figures are detected in these same vascular cells. The significance of the temporally related elevations in labeling indices of the vascular cells and the cellular constituents of the corneal cells is uncertain, but there are many potential interrelationships between the controls of cell division and migration for cells of the vessels, epithelium, endothelium, and corneal stroma.

Animals↗

Demographic and socioeconomic characteristics of Korean Americans in the United States in 1980.

"Based on the analysis of 1980 [U.S. Census] Public-Use Microdata Samples, this article demonstrates that the Korean immigrant stream, particularly men, has been very selective even before the 1965 reform.... Despite the educational superiority and somewhat positive occupational position, Korean men in the U.S. are seriously disadvantaged in income regardless of nativity status. Korean Americans are not as successful as whites in translating their education into occupation and income; they are better educated for the same job, but experience a lower income return to the same education and the same occupation."

Americas↗

Activity-dependent regulation of N-cadherin in DRG neurons: differential regulation of N-cadherin, NCAM, and L1 by distinct patterns of action potentials.

Cell adhesion molecule (CAM) expression is highly regulated during nervous system development to control cell migration, neurite outgrowth, fasciculation, and synaptogenesis. Using electrical stimulation of mouse dorsal root ganglion (DRG) neurons in cell culture, this work shows that N-cadherin expression is regulated by neuronal firing, and that expression of different CAMs is regulated by distinct patterns of neural impulses. N-cadherin was down-regulated by 0.1 or 1 Hz stimulation, but NCAM mRNA and protein levels were not altered by stimulation. L1 was down-regulated by 0.1 Hz stimulation, but not by 0.3 Hz, 1 Hz, or pulsed stimulation. N-cadherin expression was lowered with faster kinetics than L1 (1 vs. 5 days), and L1 mRNA returned to higher levels after terminating the stimulus. The RSLE splice variant of L1 was not regulated by action potential stimulation, and activity-dependent influences on L1 expression were blocked by target-derived influences. The results are consistent with changes in firing pattern accompanying DRG development and suggest that functional activity can influence distinct developmental processes by regulating the relative abundance of different CAMs.

Action Potentials↗

Methylprednisolone-induced neutrophil leukocytosis--down-modulation of neutrophil L-selectin and Mac-1 expression and induction of granulocyte-colony stimulating factor.

The mechanisms underlying corticosteroid-induced neutrophil leukocytosis are not fully understood; however, leukocyte/endothelial cell adhesion molecule interactions are known to be key to the movement of neutrophils within and out of the vasculature. This study was designed to investigate the effects of corticosteroids on neutrophil adhesion molecules in relation to neutrophil leukocytosis. Circulating neutrophil counts, neutrophil L-selectin and Mac-1 expression (measured by flow cytometry), soluble L-selectin, and granulocyte-colony stimulating factor concentrations were determined in 15 multiple sclerosis patients receiving intravenous methylprednisolone prior to and at 6 and 24 h following the initial 500-mg dose. A follow-up sample was obtained 48 h after the 5-day therapeutic course. Neutrophil counts were elevated at 6 h (threefold) and 24 h (twofold). This was associated with a 40% reduction in L-selectin expression at 6 and 24 h and a 35% reduction in Mac-1 expression at 6 h. Serum granulocyte-colony stimulating factor levels were increased (6 h: threefold; 24 h: twofold), whereas soluble L-selectin concentrations were unaltered. All of the above parameters had returned to basal levels in the follow-up sample. Short-term in vitro cultures (6 and 24 h) of blood samples from untreated multiple sclerosis patients and controls with 0.01 mg/ml methylprednisolone resulted in minimal reductions in neutrophil L-selectin and Mac-1 and no change in soluble L-selectin. Granulocyte-colony stimulating factor induced Mac-1 expression in a dose-dependent manner, whereas L-selectin expression was unaffected or reduced at high concentrations. Reduction in neutrophil L-selectin and Mac-1 expression following methylprednisolone infusion may cause decreased adhesion of marginated neutrophils and/or reduced capacity of neutrophils to migrate from the vasculature. Additionally, the induction of granulocyte-colony stimulating factor may contribute to neutrophil production and release into the circulation.

Down-Regulation↗

Regulation of protein L-isoaspartyl methyltransferase by cell-matrix interactions: involvement of integrin alphavbeta3, PI 3-kinase, and the proteasome.

The enzyme L-isoaspartyl methyltransferase (PIMT) is known to repair damaged proteins that have accumulated abnormal aspartyl residues during cell aging. However, little is known about the mechanisms involved in the regulation of PIMT expression. Here we report that PIMT expression in bovine aortic endothelial cells is regulated by cell detachment and readhesion to a substratum. During cell detachment, the PIMT level was rapidly and strongly increased and correlated with a stimulation of protein synthesis. Aside from endothelial cells, PIMT levels were also regulated by cell adhesion in various cancer cell lines. The upregulation of PIMT expression could be prevented by an anti-alphavbeta3 antibody (LM609) or by a cyclic RGD peptide (XJ735) specific to integrin alphavbeta3, indicating that this integrin was likely involved in PIMT regulation. Moreover, we found that PIMT expression returned to the basal level when cells were replated on a substratum after detachment, though downregulation of PIMT expression could be partly prevented by the PI3K inhibitors LY294002 and wortmannin, as well as by the proteasome inhibitors MG-132, lactacystin, and beta-lactone. These findings support the assumption that the PIMT level was downregulated by proteasomal degradation, involving the PI3K pathway, during cell attachment. This study reports new insights on the molecular mechanisms responsible for the regulation of PIMT expression in cells. The regulation of PIMT level upon cell-substratum contact suggests a potential role for PIMT in biological processes such as wound healing, cell migration, and tumor metastasis dissemination.

Animals↗

Sickness absence and concurrent low back and neck-shoulder pain: results from the MUSIC-Norrtälje study.

In Sweden, musculoskeletal disorders, in particular low back disorders (LBD) and neck-shoulder disorders (NSD) constitute by far the most common disorders, causing sick leave and early retirement. Studies that compare sickness absence in individuals with LBD and individuals with NSD are lacking. Moreover, it is likely that having concurrent complaints from the low back region and the neck-shoulder region could influence sickness absence. The purpose of the present study was to explore potential differences in sickness absence and in long-term sickness absence during a 5-year period, 1995-2001, among individuals with (1) solely LBD, (2) solely NSD, and (3) concurrent LBD and NSD. The present study was based on 817 subjects from the MUSIC-Norrtälje study, whom were working at baseline and whom at both baseline and follow-up reported LBD and/or NSD. Three groups were identified based on pain and pain-related disability at both baseline and follow-up: (1) solely LBD, (2) solely NSD, and (3) concurrent LBD and NSD. Subjects who did not give consistent answers at both the baseline and follow-up occasions were assigned a fourth group: (4) migrating LBD/NSD. Two outcomes were analysed: (1) prevalence of sickness absence, and (2) long-term sickness absence among those with sickness absence days. Logistic regression analysis was used to calculate odds ratios (OR) for sickness absence in the different disorder groups, taking into account confounding factors such as gender, age and other non-musculoskeletal-related disorders. In the group concurrent LBD and NSD, 59% had been sickness absent between baseline and follow up, compared to 42% in the group solely LBD, 41% in the group solely NSD, and 46% in the group migrating LBD/NSD. No difference in sickness absence was found between the group solely LBD compared to the group solely NSD [OR 0.65 (0.36-1.17)]. The adjusted OR for sickness absence in the group concurrent LBD and NSD compared to subjects with solely LBD or solely NSD was [OR 1.69 (1.14-2.51)]. The adjusted OR for having long-term sickness absence was 2.48 (95% CI = 1.32-4.66) for the group concurrent LBD and NSD. In the present study, having concurrent LBD and NSD were associated with a higher risk for sickness absence and also long-term sickness absence. This suggests that, when research on sickness absence and return to work after a period of LBD or NSD is performed, it is important to take into consideration any concurrent pain from the other spinal region. The study also implies that spinal co-morbidity is an important factor to be considered by clinicians and occupational health providers in planning treatment, or in prevention of these disorders.

Comorbidity↗

Phagocytic activity of neutrophils in human fasciolosis before and after treatment.

Neutrophil phagocytic function was studied in fifteen patients with chronic fasciolosis and five in the incubating phase of the disease. Results were compared with a control group. The chematactic index which is the ratio of directed to non directed migration, the (NBT) reduction test which estimates phagocytosis and the more recent and specific test the chemiluminescence which measures phagocytosis and intracellular killing were performed. The results showed that in fasciolosis chemotactic activity, NBT and chemiluminescence index were significantly increased as compared to controls. This increase was more prominent in the acute phase. In this stage, the immature parasites are in close contact with the liver tissue. With chronicity of infection, they reach the bile ducts and inflammation in the liver parenchyma subsides. At this stage a lower level of metabolites and antigens reach the tissues, while the majority pass with bile to the intestinal lumen. The indices returned to normal level after treatment of fasciolosis. This signifies disappearance of all stimuli responsible for activation of PMN phagocytes.

Animals↗