Low-grade Inflammatory Reaction Research Articles

The association between rheumatoid arthritis and left ventricular diastolic dysfunction: pathogenesis, predictors and managements.

Left ventricular diastolic dysfunction (LVDD) plays a central role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), a major manifestation of heart failure (HF). Low-grade inflammatory reaction is the key mechanism leading to LVDD. Rheumatoid arthritis (RA) is a systemic inflammatory disease and affects 0.5-1.0% of the adult population. Several epidemiologic studies find that the risk of LVDD is increased in RA than in the general population. Since inflammation plays an important role in the pathogenesis of LVDD and RA is a disease characterised by chronic systemic inflammation. RA may be involved in the occurrence and development of LVDD. This review summarises the pathogenesis, predictors, and management of LVDD in patients with RA.

Saikosaponin d protects pancreatic acinar cells against cerulein-induced pyroptosis through alleviating mitochondrial damage and inhibiting cGAS-STING pathway.

Acute pancreatitis represents an inflammatory disease featuring pancreatic necrosis and inflammation. Inflammatory injury of pancreatic acinar cells (PACs) is critically involved in the initiation and progression of acute pancreatitis. Pyroptosis, a new kind of programmed cell death concomitant with a low-grade inflammatory reaction, plays a function in acute pancreatitis pathology. It is unclear whether saikosaponin d (SSd), a pharmacologically active natural product, could protect PACs by regulating pyroptosis. Here, we established a PAC injury model in vitro using cerulein to treat AR42J cells. SSd restored viability and proliferation and lowered the release of pancreatic enzymes and inflammatory interleukins in cerulein-treated AR42J cells. Cerulein-induced pyroptosis was evidenced by typical ultrastructural changes and NLRP3/caspase-1 activation in AR42J cells, but SSd attenuated cerulein-induced pyroptosis and inhibited NLRP3/caspase-1 pathway. Mechanically, SSd reduced mitochondrial damage and mtDNA release, and blocked cGAS-STING signaling in AR42J cells treated with cerulein, contributing to the inhibition of NLRP3-mediated pyroptosis. Furthermore, SSd abolished cerulein-elevated oxidative stress in AR42J cells, leading to the mitigation of mitochondrial damage and inhibition of cGAS-STING signaling and pyroptosis. In conclusion, SSd protected PACs against cerulein-induced pyroptosis by alleviating mitochondrial damage and inhibiting the cGAS-STING pathway, and it could be a therapeutic candidate for acute pancreatitis.

Prevention of peritoneal adhesions formation by core-shell electrospun ibuprofen-loaded PEG/silk fibrous membrane

Adhesion bands are pathological fibrous tissues that create in the middle of tissues and organs, often reasons of intestinal obstruction, and female infertility. Here, we explored the anti-adhesive and inflammatory capacities of PEG/silk and Ibuprofen-loaded PEG/Silk core-shell nanofibrous membranes, respectively. The ibuprofen-loaded Silk Fibroin-Poly ethylene Glycol (SF-PEG) core-shell membrane was fabricated by electrospinning and considered in terms of morphology, surface wettability, drug release, and degradation. To reveal the membrane capability for adhesion bands inhibition, the membrane was stitched among the abdominal partition and peritoneum and then evaluated using two scoring adhesion systems. According to results, the fibrous membrane hindered cell proliferation, and the scoring systems and pathology showed that in a rat model, Ibuprofen-loaded PEG/Silk core-shell membrane caused a lightening in post-operative adhesion bands and the low-grade inflammatory reaction in animal models. Collectively, we fabricated new ibuprofen-loaded PEG/SF membranes with anti-adhesion and anti-inflammation properties. Moreover, this core-shell electrospun fibrous membrane has not even now been used to prevent peritendinous adhesion generation.

Can Red cell distribution width screen for metabolic abnormality in women with Polycystic Ovarian Syndrome?

Polycystic ovarian syndrome (PCOS) is a prevalent endocrinopathy in reproductive-age females, accredited to a chronic low-grade inflammatory reaction. Red distribution width (RDW), a parameter of complete blood count, was tested as an inflammatory marker ; higher RDW was linked to metabolic syndrome. We aimed to examine RDW in distinguishing PCOS-related metabolic and hormonal abnormalities. Methods : A case-control study recruited 128 women, divided into PCOS cases (64 / 128) and controls (64 / 128) according to Rotterdam criteria. Body mass index (BMI), estimated complete blood count parameters, hormonal markers (serum follicle-stimulating hormone (FSH), luteinizing hormone, and serum testosterone), and metabolic markers (HOMA-IR, serum high and low-density lipoprotein) were measured. Results showed that RDW was significantly higher in PCOS. HOMA-IR, LDL, testosterone, and LH / FSH were higher in PCOS and strongly correlated with RDW with positive correlations. HDL was elevated and correlated negatively with RDW in PCOS. ROC calculated (13.55) as RDW cut-off value for insulin-resistant with an AUC of 0.95, P < 0.001. In conclusion, a strong and remarkable correlation of RDW with metabolic abnormalities in PCOS cases with 100% sensitivity and specificity, in addition to being quick and inexpensive, makes it a reliable marker for screening for insulin resistance. J. Med. Invest. 69 : 191-195, August, 2022.

Serum Heparanase: A New Clinical Biomarker Involved in Senile Metabolic Inflammatory Syndrome.

AimMetabolic inflammation syndrome (MIS) can lead to a series of complications, but its exact inflammatory mechanism is still unclear. The aim of this study was to explore the correlation between heparanase (HPA) and MIS, and the close relationship between HPA and other chronic low-grade inflammation index, such as C-reactive protein (CRP) and interleukin-6 (IL-6).MethodsA total of 105 patients with MIS in the physical examination population of Huashan Hospital affiliated to Fudan University from May to June 2018 were selected as the MIS group, and 52 patients who were relatively healthy during the same period were used as the control group. The basic clinical data of the selected candidates were collected, the levels of serum HPA, CRP and IL-6 were measured by ELISA, and the levels of blood glucose and blood lipids were also detected.ResultsCompared with the control group, the levels of HPA, CRP, IL-6, FBG, HbA1C, and TG of MIS group were all significantly elevated (all P<0.05), and HDL-C levels were considerably reduced (P<0.05). Correlation analysis showed that there was a noticeably positive correlation between serum HPA level and CRP, IL-6 levels (P<0.05).ConclusionHigher HPA levels might play a certain role in the occurrence and development of MIS. There was a certain close correlation between serum HPA level and CRP and IL-6 levels, and which indicated that HPA was involved in the chronic low-grade inflammatory reaction process of MIS.

Relationships among oncostatin M, insulin resistance, and chronic inflammation: a pilot study.

Objective Activated macrophages (M1-type macrophages) in adipose tissue secrete many proinflammatory cytokines that induce insulin resistance (IR). Oncostatin M (OSM), a member of the interleukin-6 (IL-6) family of Gp130 cytokines, plays an important role in a variety of biological functions, including the regulation of inflammatory responses. Proinflammatory cytokines released in patients with IR trigger a chronic, low-grade inflammatory reaction in blood vessel walls. This inflammator response leads to endothelial damage, which is the main mechanism for atherosclerosis and many cardiovascular diseases. Animal studies have reported a relationship between OSM and IR. To the best of our knowledge, however, few clinical studies have examined this topic. Therefore, we studied the relationship between serum levels of OSM and IR. Subjects and methods This prospective cross-sectional case-control study enrolled 50 people with IR (according to the HOMA-IR and QUICKI indices) and 34 healthy controls. The fasting blood concentrations of insulin, glucose, blood urea nitrogen (BUN), creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglyceride, total cholesterol, C-reactive protein (CRP), and OSM were determined. Results There were no significant differences between the two groups in age, sex, and HbA1c levels. Univariate analyses showed that waist circumference (WC) and levels of fasting glucose, insulin, CRP, HDL-C, OSM, HOMA-IR, and QUICKI differed between the two study groups. In multivariate analyses, both IR indices (QUICKI and HOMA) and OSM differed between the two groups. Conclusion OSM was correlated with the IR indices (QUICKI and HOMA). For simplicity, it might replace the other IR indices in the future. Further detailed studies are needed to confirm this.

Biomarkers of Inflammation in Left Ventricular Diastolic Dysfunction.

Left ventricular diastolic dysfunction (LVDD) is an important precursor to many different cardiovascular diseases. Diastolic abnormalities have been studied extensively in the past decade, and it has been confirmed that one of the mechanisms leading to heart failure is a chronic, low-grade inflammatory reaction. The triggers are classical cardiovascular risk factors, grouped under the name of metabolic syndrome (MetS), or other systemic diseases that have an inflammatory substrate such as chronic obstructive pulmonary disease. The triggers could induce myocardial apoptosis and reduce ventricular wall compliance through the release of cytokines by multiple pathways such as (1) immune reaction, (2) prolonged cell hypoxemia, or (3) excessive activation of neuroendocrine and autonomic nerve function disorder. The systemic proinflammatory state causes coronary microvascular endothelial inflammation which reduces nitric oxide bioavailability, cyclic guanosine monophosphate content, and protein kinase G (PKG) activity in adjacent cardiomyocytes favoring hypertrophy development and increases resting tension. So far, it has been found that inflammatory cytokines associated with the heart failure mechanism include TNF-α, IL-6, IL-8, IL-10, IL-1α, IL-1β, IL-2, TGF-β, and IFN-γ. Some of them could be used as diagnosis biomarkers. The present review aims at discussing the inflammatory mechanisms behind diastolic dysfunction and their triggering conditions, cytokines, and possible future inflammatory biomarkers useful for diagnosis.

CD18 Regulates Monocyte Hematopoiesis and Promotes Resistance to Experimental Schistosomiasis.

Infection with Schistosoma mansoni causes a chronic parasitic disease that progress to severe liver and gastrointestinal damage, and eventually death. During its development into mammalian hosts, immature schistosomula transit through the lung vasculature before they reach the liver to mature into adult worms. A low grade inflammatory reaction is induced during this process. However, molecules that are required for efficient leukocyte accumulation in the lungs of S. mansoni-infected subjects are unknown. In addition, specific leukocyte subsets that mediate pulmonary response during S. mansoni migration through the lung remain to be elucidated. β2 integrins are fundamental regulators of leukocyte trans-endothelial migration and function. Therefore, we investigated their role during experimental schistosomiasis. Mice that express low levels of CD18 (the common β2 integrin subunit) and wild type C57BL/6 mice were subcutaneously infected with S. mansoni cercariae. Cellular profiles of lungs and livers were evaluated in different time points after infection by flow cytometry. Low levels of CD18 affected the accumulation of patrolling Ly6Clow, intermediate Ly6Cinter monocytes, monocyte-derived macrophages and monocyte-derived dendritic cells in the lungs 7 days after infection. This correlated with increased TNF-α levels. Strikingly, low CD18 expression resulted in monocytopenia both in the peripheral blood and bone marrow during acute infection. After 48 days, S. mansoni worm burdens were higher in the hepatic portal system of CD18low mice, which also displayed reduced hepatic accumulation of patrolling Ly6Clow and intermediate Ly6Cinter, but not inflammatory Ly6Chigh monocytes. Higher parasite burden resulted in increased granulomatous lesions in the liver, increased egg deposition and enhanced mortality. Overall, our data point for a fundamental role of CD18 for monocyte hematopoiesis during infection, which promotes an efficient host response against experimental schistosomiasis.

Abstract 354: Sirt1 Negatively Regulates Cardiac Inflammation Induced by Metabolic Stress

Obesity is a major risk factor for heart disease. Metaflammation is a metabolically driven, chronic, low-grade inflammatory reaction that is seen in the heart under obese conditions. Cardiac myocytes are known to produce inflammatory cytokines such as interleukin-6 (IL-6). However, whether and how cardiac myocytes mediate metaflammation is unknown. Silent information regulator 1 (Sirt1), a histone deacetylase involved in numerous metabolic pathways, facilitates an anti-inflammatory function through inhibition and deacetylation of the NFkB p65 subunit. This project aims to examine whether Sirt1 plays a role in cardiac local metaflammation. Mice with cardiac specific Sirt1 gene deletion (c-Sirt1 KO), Sirt1 overexpression (Tg-Sirt1), and relevant controls (Flox/Flox and WT respectively) were each placed on high fat and regular chow diets. The mice were euthanized after 3 months and their hearts were extracted for genetic and molecular analyses. Sirt1 mRNA and protein levels were significantly decreased under HFD feeding conditions (50% reduction in HFD feeding compared to normal diet, P&lt;0.05). Acetylation of p65 was significantly induced by HFD feeding, and was further enhanced in c-Sirt1 KO mice, but inhibited in Tg-Sirt1 mice. Cardiac inflammation was enhanced in the c-Sirt1 KO group as evidenced by a significant increase in mRNA levels of IL-6 in mice fed regular chow (3-fold increase in c-Sirt1 KO vs. Sirt1 Flox/Flox, p&lt;0.05) and HFD (5-fold increase in c-Sirt1 KO vs. Sirt1 Flox/Flox, p&lt;0.05). Intracellular IL-6 signaling steps, such as phosphorylation of STAT3, were enhanced in c-Sirt1 KO, but inhibited in Tg-Sirt1 mice under HFD feeding conditions. These results suggest that cardiac myocytes mediate metaflammation partly through downregulation of Sirt1.

Dexamethasone intravitreal implant in the treatment of diabetic macular edema.

Diabetic macular edema (DME) resembles a chronic, low-grade inflammatory reaction, and is characterized by blood–retinal barrier (BRB) breakdown and retinal capillary leakage. Corticosteroids are of therapeutic benefit because of their anti-inflammatory, antiangiogenic, and BRB-stabilizing properties. Delivery modes include periocular and intravitreal (via pars plana) injection. To offset the short intravitreal half-life of corticosteroid solutions (~3 hours) and the need for frequent intravitreal injections, sustained-release intravitreal corticosteroid implants have been developed. Dexamethasone intravitreal implant provides retinal drug delivery for ≤6 months and recently has been approved for use in the treatment of DME. Pooled findings (n=1,048) from two large-scale, randomized Phase III trials indicated that dexamethasone intravitreal implant (0.35 mg and 0.7 mg) administered at ≥6-month intervals produced sustained improvements in best-corrected visual acuity (BCVA) and macular edema. Significantly more patients showed a ≥15-letter gain in BCVA at 3 years with dexamethasone intravitreal implant 0.35 mg and 0.7 mg than with sham injection (18.4% and 22.2% vs 12.0%). Anatomical assessments showed rapid and sustained reductions in macular edema and slowing of retinopathy progression. Phase II study findings suggest that dexamethasone intravitreal implant is effective in focal, cystoid, and diffuse DME, in vitrectomized eyes, and in combination with laser therapy. Ocular complications of dexamethasone intravitreal implant in Phase III trials included cataract-related events (66.0% in phakic patients), intraocular pressure elevation ≥25 mmHg (29.7%), conjunctival hemorrhage (23.5%), vitreous hemorrhage (10.0%), macular fibrosis (8.3%), conjunctival hyperemia (7.2%), eye pain (6.1%), vitreous detachment (5.8%), and dry eye (5.8%); injection-related complications (eg, retinal tear/detachment, vitreous loss, endophthalmitis) were infrequent (<2%). Dexamethasone intravitreal implant offers a viable treatment option for DME, especially in cases that are persistent or treatment (anti-vascular endothelial growth factor/laser) refractory.

Orange juice intake during a fatty meal consumption reduces the postprandial low-grade inflammatory response in healthy subjects

Background and AimsEvidence associates polyphenol-rich foods to reduction of low-grade inflammation and mortality for cardiovascular disease, the mechanisms underlying such effects being still unclear. Consumption of a fatty meal by healthy volunteers induces rapid and reversible low-grade inflammation. The aim of the present study was to evaluate the effect of orange juice on cellular modifications induced by a fatty meal. Methods and Results18 apparently healthy subjects consumed a fatty meal, during which they drunk orange juice, either blond or red, or water, according to a randomized cross-over design. Two hours after the end of the fatty meal, both white blood cell (WBC) and platelet counts significantly increased (12.5 and 5 %, respectively), while mean platelet volume decreased and a 25% release of myeloperoxidase (MPO) from polymorphonuclear leukocyte occurred. Both juices significantly prevented WBC increase and MPO degranulation, in respect to control. Triglycerides significantly increased (42%) after the fatty meal, but at a lower extent when red orange juice was consumed with the meal (20%), in respect to blond orange juice or control. This effect was statistically significant in the subgroup of 8 subjects with hypertriglyceridemia. Vascular stiffness (augmentation index), measured by Endo-PAT2000, significantly decreased after the meal only in conjunction with red orange juice. ConclusionIn healthy subjects the concomitant intake of orange juice may prevent the low-grade inflammatory reaction induced by a fatty meal, at cellular and possibly at vascular function levels. The relative role of different polyphenols on the observed effects of orange juices remains to be established.

The microcirculation in adipose tissue inflammation

In most humans, obesity is associated with a chronic low-grade inflammatory reaction occurring in several organ tissues, including the adipose tissue. Infiltration of bone marrow derived leukocytes (granulocytes, monocytes, lymphocytes) into expanding adipose depots appears to be an integral component of inflammation in obesity. Circulating leukocytes invade organ tissues mainly through post-capillary venules in the microcirculation. The endothelium of the post-capillary venules acts as a gatekeeper to leukocyte adhesion and extravasation by displacing on its luminal surface adhesion molecules that bind the adhesive receptors expressed on circulating leukocytes. Several studies investigating the impact of obesity on the microcirculation have demonstrated the occurrence of microvascular dysfunction in experimental animal model of obesity, as well as in obese humans. To date though, working hypotheses and study designs have favored the view that microvascular alterations are secondary to adipose tissue dysfunction. Indeed, a significant amount of data exists in the scientific literature to support the concept that microvascular dysfunction may precede and cause adipose tissue inflammation in obesity. Through review of key published data, this article prospectively presents the concept that in response to nutrients overload the vascular endothelium of the microcirculation acutely activates inflammatory pathways that initiate infiltration of leukocytes in visceral adipose tissue, well before weight gain and overt obesity. The anatomical and physiological heterogeneity of different microcirculations is also discussed toward the understanding of how obesity induces different inflammatory phenotypes in visceral and subcutaneous fat depots.

Source of inflammatory markers in patients with atrial fibrillation

Elevated levels of C-reactive protein and other inflammatory markers have been reported in some patients with atrial fibrillation (AF). Whether this finding is related to AF per se or to other conditions remains unclear. In addition, the source of inflammatory markers is unknown. Therefore, in the present study, we sought to assess the extent and the source of inflammation in patients with AF and no other concomitant heart or inflammatory conditions. The study group consisted of 29 patients referred for radiofrequency catheter ablation: 10 patients with paroxysmal AF, 8 patients with permanent AF, and 10 control patients with Wolf-Parkinson-White (WPW) syndrome and no evidence of AF (mean age 54 +/- 11 vs. 57 +/- 13 vs. 43 +/- 16). No patient had structural heart diseases or inflammatory conditions. High-sensitive C-reactive protein, interleukin-6 (IL-6), and interleukin-8 (IL-8) were assessed in blood samples from the femoral vein, right atrium, coronary sinus, and the left and right upper pulmonary veins. All samples were collected before ablation. Compared with controls and patients with paroxysmal AF, patients with permanent AF had higher plasma levels of IL-8 in the samples from the femoral vein, right atrium, and coronary sinus, but not in the samples from the pulmonary veins (median values in the femoral vein: 2.58 vs. 2.97 vs. 4.66 pg/mL, P = 0.003; right atrium: 2.30 vs. 3.06 vs. 3.93 pg/mL, P = 0.013; coronary sinus: 2.85 vs. 3.15 vs. 4.07, P = 0.016). A high-degree correlation existed between the IL-8 levels in these samples (correlation coefficient between 0.929 and 0.976, P < 0.05). No differences in the C-reactive protein and IL-6 levels were noted between the three groups of patients. The normal levels of C-reactive protein and IL-6, along with the elevated levels of IL-8 in patients with permanent AF but not in those with paroxysmal AF, suggest a link between a low-grade inflammatory reaction and long-lasting AF. The elevated IL-8 levels in the peripheral blood, right atrium, and coronary sinus but not in the pulmonary veins suggest a possible source of inflammation in the systemic circulation.

Monomeric tartrate resistant acid phosphatase induces insulin sensitive obesity.

BackgroundObesity is associated with macrophage infiltration of adipose tissue, which may link adipose inflammation to insulin resistance. However, the impact of inflammatory cells in the pathophysiology of obesity remains unclear. Tartrate resistant acid phosphatase (TRAP) is an enzyme expressed by subsets of macrophages and osteoclasts that exists either as an enzymatically inactive monomer or as an active, proteolytically processed dimer.Principal FindingsUsing mice over expressing TRAP, we show that over-expression of monomeric, but not the dimeric form in adipose tissue leads to early onset spontaneous hyperplastic obesity i.e. many small fat cells. In vitro, recombinant monomeric, but not proteolytically processed TRAP induced proliferation and differentiation of mouse and human adipocyte precursor cells. In humans, monomeric TRAP was highly expressed in the adipose tissue of obese individuals. In both the mouse model and in the obese humans the source of TRAP in adipose tissue was macrophages. In addition, the obese TRAP over expressing mice exhibited signs of a low-grade inflammatory reaction in adipose tissue without evidence of abnormal adipocyte lipolysis, lipogenesis or insulin sensitivity.ConclusionMonomeric TRAP, most likely secreted from adipose tissue macrophages, induces hyperplastic obesity with normal adipocyte lipid metabolism and insulin sensitivity.

Role of Glucoxidation and Lipid Oxidation in the Development of Atherosclerosis

Previous data have indicated that modification of proteins/lipids by glucoxidation and/or lipid oxidation may initiate/propagate the formation of atherosclerotic plaques. Although the biomarker carboxymethyllysine (CML) has been detected in these lesions, the origin of the reactive oxygen species (ROS) leading to its formation and the source of its carbon backbone are unknown. As presented here, the stimulation of cultured monocytes by phorbol-12-myristate-13-acetate (TPA), an activator of protein kinase C that can mimic the effects of high glucose, angiotensin II, and other physiological stimuli, leads to cellular ROS generation and concomitant formation of intracellular CML. Inhibitors of ROS-generating cellular systems such as NO synthase, xanthine oxidase, or cytochrome P450 oxidase had no effect on CML formation. Likewise, in cells with inactive NAD(P)H oxidase no reduced CML formation was found. In cells exhibiting a high glycolysis rate, CML formation was unaffected. Because we found rapid CML formation in the presence of unsaturated fatty acids, it appears that lipid oxidation is quantitatively more important. In vivo studies revealed strong intracellular CML staining in areas of histiocytic/monocytic infiltration or proliferation, mostly associated with atheroma formation. Corresponding CML staining patterns were found in healing wounds of different ages, indicating that formation of atherosclerosis is a chronic wound repair associated with a low-grade inflammatory reaction. In summary, CML is formed concomitantly with oxidative stress in activated monocytes and can be regarded as a biomarker for a low-grade inflammatory tissue reaction in the atherosclerotic plaque. Its formation via lipid oxidation may be involved in the development of atherosclerosis.

Arterial endothelial injury due to infection in childhood: ticking bomb or innocent bystander?

Atherosclerosis is regarded as a chronic disease that begins in early life. While the main underlying mechanism of atherosclerosis is nowadays unequivocally attributed to a low-grade inflammatory reaction, the spectrum of aetiological conditions is far from being fully elucidated. Both viruses and bacteria have been suggested to intervene at various stages of atherosclerosis development, although a clear pathogenic link between infection and atherosclerosis remains debatable. As one key event in atherogenesis involves a perturbation of the protective mechanisms normally posed by the arterial endothelium, a number of studies have enquired into the possible detrimental effects of microbes and their components on the endothelial cells. This review aims to scrutinize the current literature in this regard, and to suggest several possible directions for future studies.

Arterial endothelial injury due to infection in childhood: ticking bomb or innocent bystander?

Atherosclerosis is regarded as a chronic disease that begins in early life. While the main underlying mechanism of atherosclerosis is nowadays unequivocally attributed to a low-grade inflammatory reaction, the spectrum of aetiological conditions is far from being fully elucidated. Both viruses and bacteria have been suggested to intervene at various stages of atherosclerosis development, although a clear pathogenic link between infection and atherosclerosis remains debatable. As one key event in atherogenesis involves a perturbation of the protective mechanisms normally posed by the arterial endothelium, a number of studies have enquired into the possible detrimental effects of microbes and their components on the endothelial cells. This review aims to scrutinize the current literature in this regard, and to suggest several possible directions for future studies.

Metabolic aspects of continuous renal replacement therapies

Metabolic aspects of continuous renal replacement therapies

Schizotrypanids: the occurrence of dermatitis in immunodeficient animals infected with Trypanosoma cruzi.

Congenitally athymic nude Balb/c (nu/nu) and their phenotypically normal adult and neonate littermates (nu/+), the C3H/HeN as well, were intraperitoneally infected with two strains (Y or CL) or Trypanosoma cruzi. The nude mice and the neonates developed a severe parasitaemia, the susceptible C3H/HeN also presented high level and adult Balb/c mice presented parasitaemia similar to that observed in outbred mice. Erythematous skin lesions were observed initially in infected athymic nude and neonates, being characterized by nests of amastigotes in the dermis; in C3H/HeN infected mice no nest of parasite was observed but a low-grade inflammatory reaction was seen. In adult Balb/c or OF1 outbred mice nest was found but discreet inflammatory reaction was observed in severe infections.

Studies of bovine farcy in the Sudan: I. Pathology of the disease

A disease survey involving some hundreds of animals was carried out in 1958, 1959 and 1963 in the Sudan to study bovine farcy. Animals in the Quarantine Station at Khartoum North and in some abattoirs were also examined. A full description is given of the distribution of lesions and the accompanying symptoms. The disease progressed very slowly and painlessly and occurred in the chronic form only. Clinically it was characterised by tumefaction and granulomatous inflammation of the superficial lymph nodes, the vessels and the subcutis, with suppuration at a later stage. The histopathological changes were characteristic and indicated a low grade inflammatory reaction.