[Suppurative inflammation of the inner ear, abscess of the cerebellum and thrombosis of the sigmoid sinus as a complication of chronic inflammation of the middle ear].
Explore the source record for details and available documents.
Abscess↗
SEARCH · Search PubMed
Results for “INFLAMMATION”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Biological properties of Ureaplasma urealyticum and Mycoplasma hominis isolated from patients with urethral inflammations. III. Occurrence of serological types of U. urealyticum among the strains isolated from healthy men those with urethral inflammations, and their sexual partners].
Explore the source record for details and available documents.
Adult↗
[Biological properties of Ureaplasma urealyticum and Mycoplasma hominis isolated from patients with urethral inflammations. IV. Occurrence of serological variants of M. hominis among the strains isolated from healthy men those with urethral inflammations and their sexual partners].
Explore the source record for details and available documents.
Adult↗
[Plastic cast obturators of the auditory canal for the prevention of recurring auditory canal inflammations or chronic middle ear inflammations in active swimmers].
Explore the source record for details and available documents.
Chronic Disease↗
[Effect of absorbed fluorides on gingival inflammation and relation of plague to the degree of alveolysis, of deep migration of epithelial attachment and of gingival inflammation in white rats].
Explore the source record for details and available documents.
Alveolar Process↗
Studies on causal relations in endogenous, non-purulent, ocular inflammations. Observations in a sample of four hundred and twenty patients with various ocular inflammations, compared with findings in a control group of two hundred and nine people.
Explore the source record for details and available documents.
Endophthalmitis↗
[Current data on the etiology of inflammation, rheumatoid inflammation in particular].
Explore the source record for details and available documents.
Arthritis, Rheumatoid↗
[Biochemical studies on inflammation of the lungs. I. Changes in the content and composition of proteins, in the content of nucleic acids and cathepsin activity in the lungs of rabbits during a severe acute inflammation of the lungs caused by inhalation of diazomethane].
Explore the source record for details and available documents.
Animals↗
Crystal induced inflammation in canine joints. 3. Evidence against bradykinin as a mediator of inflammation.
Explore the source record for details and available documents.
Animals↗
Joint inflammations as complications in intestinal inflammations.
Ulcerative colitis and regional ileitis may be accompanied by articular involvement as extraintestinal complications, and were observed in 11 and 4 patients respectively. The temporal connection between the intestinal diseases and the appearance of subsidence of these complications in the majority of the cases suggest an etiologic relationship, regardless of the fact that the etiology of the intestinal diseases has not yet been elucidated. The clinical picture and course as well as the laboratory findings indicate that the joint involvement in question differs from rheumatoid arthritis.
Adolescent↗
Laparoscopic cholecystectomy for acute inflammation of the gallbladder.
OBJECTIVE: The aim of this study was to prospectively assess the results of laparoscopic cholecystectomy in patients with acute inflammation of the gallbladder. SUMMARY BACKGROUND DATA: Laparoscopic cholecystectomy has become the standard treatment for symptomatic gallbladder disease. Its role in the surgical treatment of acute cholecystitis has not been defined, although a number of recent reports suggest that there should be few contraindications to an initial laparoscopic approach. METHODS: All patients presenting with symptomatic cholelithiasis from October 1990 until June 1992 were evaluated at laparoscopy with intention of proceeding to a laparoscopic cholecystectomy. The gross appearance of the gallbladder was categorized as acute inflammation, chronic inflammation, or no inflammation. Ninety-eight (23.4%) of 418 patients had acute inflammation of the gallbladder: 55 were edematous, 10 were gangrenous, 15 had a mucocele, and 18 had an empyema. RESULTS: The authors assessed outcome in these patients. The frequency of conversion to an open operation was 33.7% for acute inflammation, 21.7% for chronic inflammation (p < 0.05), and 4% for no inflammation (p < 0.001). The conversion rate was highest for empyema (83.3%) and gangrenous cholecystitis (50%), while the conversion rate for edematous cholecystitis was 21.8% and for acute inflammation with a mucocele it was 7%. The median operation time for successful laparoscopic cholecystectomy for acute inflammation was 105 minutes, which was longer than that with no inflammation (90 minutes). However, the incidence of complications was not different from that for chronic or no inflammation. The median postoperative stay for patients with acute gallbladder inflammation was 2 days for successful laparoscopic cholecystectomy and 7 days for patients converted to an open operation. CONCLUSIONS: Laparoscopic cholecystectomy for acute inflammation of the gallbladder is safe and is associated with a significantly shorter postoperative stay compared to open surgery. A greater number of patients required conversion to open operation compared to those with no obvious inflammation. Conversion to open operation was most frequent for empyema and gangrenous cholecystitis, suggesting that once this diagnosis is made, excessive time should not be spent in laparoscopic trial dissection before converting to an open operation.
Acute Disease↗
Acute inflammation of the knee joint in the cat alters responses of flexor motoneurons to leg movements.
1. This is a report of changes in reflex excitability of flexor motoneurons in response to innocuous mechanical stimuli following initiation of an acute experimental inflammation of the knee joint in the chloralose-anaesthetized cat spinalized at level T12. 2. Activity of functionally single alpha- or gamma- motoneurons, identified by ventral root stimulation, was recorded in filaments of the nerve to biceps semitendinosus before and after onset of an acute inflammation. The inflammation was evoked by injection into the knee cavity of the compounds kaolin and carrageenan. 3. Measurements were made of resting activity, responses to local pressure applied to parts of the upper or lower limb, and to flexion or extension movements at the knee joint before and after onset of the inflammation. In two experiments, one in which no inflammation was initiated, and another in which recordings were made only after the inflammation had fully developed, a survey of large numbers of neurons (44 alpha and 84 gamma) showed that under control conditions only 14% of alpha-motoneurons showed a response to mechanical stimulation compared with 41% of gamma-motoneurons. In the presence of an inflammation 41% of alpha-cells were responsive compared with 64% of gamma-cells. 4. Inflammation-induced changes in activity of motoneurons including both excitatory and inhibitory effects, took 1-2 h to fully develop. Excitatory effects included a rise in resting discharge, an increase in the response to local pressure, and an increased response to flexion and/or to extension of the knee. Inhibitory effects included falls in resting discharge and/or in the responses to leg movements. 5. For 35 cells identified as alpha-motoneurons and tested both before and after initiation of an inflammation, 20 remained unresponsive throughout the experiment, whereas 4 that had not responded during the control period began after inflammation to respond to local pressure and/or flexion/extension movements. Of 11 units that exhibited some response before inflammation, 8 showed an increase with inflammation, whereas 2 became unresponsive. 6. The inflammation had rather more dramatic effects on gamma-neurons. Many showed control responses to leg movements, and these were measurably modified by inflammation. Of 56 gamma-cells tested under control conditions, 26 were unresponsive to all stimuli, whereas 30 showed some form of response including activity during flexion and extension movements of the leg. Where responses were tested both before and after onset of an inflammation, 11 of 13 unresponsive units remained unresponsive.(ABSTRACT TRUNCATED AT 400 WORDS)
Acute Disease↗
Inflammation in prostate biopsies of men without prostatic malignancy or clinical prostatitis: correlation with total serum PSA and PSA density.
OBJECTIVE: Inflammation is a frequent histological finding in prostate biopsies, performed on men without prostatic malignancy or clinical prostatitis. We investigated the relationship between morphological parameters of inflammation in prostatic tissue and total serum prostate-specific antigen (PSA) and prostate-specific antigen density (PSAD) levels to determine if subclinical inflammation can cause elevation of PSA and PSAD. METHODS: We reviewed 268 prostate biopsies, performed on 238 men with elevated PSA and/or abnormal digital rectal examination of the prostate. All premalignant and malignant biopsies and cases of clinical prostatitis were excluded. The inflammation in the remaining 145 prostate biopsies was scored for extent of inflammation and aggressiveness of inflammation, using the four-point scale designed by Irani and co-workers. In this prostatic inflammation scoring system, extent of inflammation is graded from 0 up to 3 according to the degree of invasion of inflammatory cells in prostatic tissue. Aggressiveness of inflammation is graded from 0 up to 3 according to the degree of contact or disruption of prostatic glandular epithelium by inflammatory cells. RESULTS: Each of the studied biopsies showed inflammatory cells. Median PSA levels in grades 1, 2 and 3 of extent of inflammation were, respectively, 5.7, 6.8 and 13. 0. Median PSAD levels in these groups were 0.13, 0.16 and 0.33. There was no significant difference between these grades for PSA nor for PSAD. Median PSA levels in grades 0, 1 and 2 of aggressiveness of inflammation were, respectively, 3.9, 5.9 and 8.9. Median PSAD levels in these groups were 0.12, 0.18 and 0.17. For both parameters, there was a significant difference between grades (respectively, p = 0.0028 and p = 0.0330). CONCLUSION: Inflammation of the prostate is a histological finding in almost every set of prostate biopsies, even when there are no signs of clinical prostatitis. This subclinical inflammation can cause PSA elevation. Not the extent of inflammation is of importance, but the disruption of epithelial integrity caused by the inflammatory infiltrate. When confronted with a patient with an elevated PSA level whose prostate biopsies reveal no malignancy but only inflammation, this concept can help in determining the need for quick repeat biopsies.
Acute Disease↗
Systemic and local inflammation in patients with unstable atherosclerotic plaques.
The response to injury in the vasculature and the heart is inflammation. Atherosclerosis is often the result of injury followed by inflammation and atherosclerosis. Vascular and myocardial infections from various pathogens, including viruses, bacteria, chlamydia, and other infections result in vascular inflammation and almost certainly play a role in the development of atherosclerosis and acute coronary heart disease syndromes in at least some patients. Current evidence favors prior exposure to multiple pathogens as most likely playing a role in initiating inflammation and contributing to atherosclerosis. Genetic predisposition is almost certainly an important factor in the development of inflammation, impaired endothelial vascular repair, vascular infection, thrombosis, and atherosclerosis. The aging process itself is most likely associated with altered vascular and myocardial defense mechanisms predisposing to inflammation. The oxidation of cholesterol and low-density lipoprotein (LDL) leads to the production of oxidized radicals that promote vascular inflammation. Interventional injury, including angioplasty and stenting, causes endothelial inflammation, thrombosis, and fibroproliferation. Systemic evidence of inflammation identifies patients at high risk of future coronary events, including those who appear to be healthy initially as well as those with stable and unstable coronary heart disease syndromes. Increases in serum C-reactive protein (CRP) identify individuals at risk for future vascular events, including unstable angina, acute myocardial infarction, acute cerebrovascular accident, and sudden death. Similarly, systemic elevations in serum troponin 1, serum amyloid-like protein, fibrinogen, and interleukins-1, 2, 6, 8, and 18 identify patients with unstable angina and non-Q-wave myocardial infarction at increased risk for future coronary events. The presence of vascular inflammation may be detected by identifying temperature heterogeneity within plaques that demonstrate inflammation. In the future, the local evaluation of atherosclerotic plaques to detect the presence of inflammation coupled to measurements of systemic markers of inflammation, such as C-reactive protein, may help identify patients at increased risk and allow both local and systemic therapies that reduce their risk and prevent the development of acute coronary syndromes in at least some patients.
Arteriosclerosis↗
Enhancement of the responses of ascending tract cells in the cat spinal cord by acute inflammation of the knee joint.
Recordings were made from 16 ascending tract cells in the spinal cords of anaesthetized, spinalized cats before and after an acute arthritis was produced by injection of kaolin and carrageenan into the knee joint. The responses tested routinely were to passive flexion of the knee, an innocuous movement. In some cases, responses to other movements were also tested, and changes in background discharge rates were monitored. Control recordings for a period of 1 h or in 3 cases of 3 h indicated that the responses to flexion were reasonably stationary. Four tract cells that initially showed little or no response to flexion of the knee joint developed large responses within 1 to 2 h after inflammation of the joint. Another 9 cells were tested that had responses to flexion of the knee joint prior to inflammation. In 6 cases, inflammation produced enhanced static or transient responses. In 2 cases, the effect of flexion was initially inhibitory or variable, but after inflammation these cells showed large excitatory responses. In the other case, inflammation had no effect. Background discharges were increased by inflammation in 6 of these 9 cells. The effect of inflammation of the knee joint was tested on 3 tract cells that had no clearly defined receptive field in the knee. In 1 case, a response developed to knee flexion after acute inflammation was produced. In the other 2 cases, there were initially responses to knee flexion, but these were unchanged by inflammation. Two of the cells tested had bilateral receptive fields in or around the knee joints. Inflammation of one knee joint enhanced the responses to flexion of the same but not of the contralateral knee in one case but greatly increased the responses to flexion of both knees in the other case. Injections of prostaglandin (PGE2) caused an enhancement of the responses to knee flexion beyond that caused by inflammation in 5 of 7 cases. One cell whose responses to flexion of the knee were unaffected by inflammation showed inhibitory responses to prostaglandin injections into the inflamed knee joint. The effects of inflammation on the responses of ascending tract cells of the spinal cord appear to serve as a useful neural model of the events responsible for the development of arthritic pain.
Acute Disease↗
The influence of chronic inflammation in prostatic carcinogenesis: a 5-year followup study.
PURPOSE: We investigated an association between chronic prostatic inflammation and prostate carcinogenesis. MATERIALS AND METHODS: Initial prostate needle biopsies from 177 patients with clinical parameters suspicious for malignancy were examined. We evaluated them for the presence and extent of chronic inflammation and other pathological findings. Findings in followup biopsies during the next 5 years were reviewed and correlated with the initial results. RESULTS: Two patients subset were identified, including 144 patients with and 33 without chronic inflammation in the initial biopsies. Additional pathological findings in some cases in each group included simple atrophy, high grade prostatic intraepithelial neoplasia, adenocarcinoma and atypical small acinar proliferation. Post-atrophic hyperplasia and proliferative inflammatory atrophy were noted only in patients with chronic inflammation. A significant association between serum prostate specific antigen and the degree of inflammation was observed in needle biopsies. In repeat biopsies within 5 years in patients with chronic inflammation 29 new cancers were diagnosed, representing a new cancer incidence of 20%. Of these cancers 6 occurred in patients in whom initial biopsies showed only chronic inflammation, 15 occurred in patients with initial post-atrophic hyperplasia/proliferative inflammatory atrophy lesions, 7 occurred in patients with initial high grade prostatic intraepithelial neoplasia and chronic inflammation, and 1 occurred in a patient with initial atypical small acinar proliferation and chronic inflammation. High grade prostatic intraepithelial neoplasia was newly discovered in 9 patients in the initial chronic inflammation group, of whom 7 had post-atrophic hyperplasia/proliferative inflammatory atrophy and 2 had simple atrophy and chronic inflammation in the initial biopsies. In contrast, in 33 patients initially showing no inflammation adenocarcinoma was subsequently found in 2 (6%). One of these patients had high grade prostatic intraepithelial neoplasia and the other had atypical small acinar proliferation on initial biopsies. CONCLUSIONS: Chronic inflammation may be a significant risk factor for prostatic adenocarcinoma.
Adenocarcinoma↗
Altered ruminal microbiome tryptophan metabolism and their derived 3-indoleacetic acid inhibit ruminal inflammation in subacute ruminal acidosis goats.
BACKGROUND: Subacute ruminal acidosis (SARA) is a digestive disorder that often severely jeopardizes the health and lactation performance of ruminants fed a high-energy diet. Different dairy ruminants exhibit varying degrees of inflammation accompanied by variations in the rumen microbiota when SARA occurs. Our understanding of the occurrence of SARA and varying degrees of rumen epithelial inflammation is lacking. Hence, we performed rumen metagenomic, metagenome-assembled genome and metabolomic analyses, with transcriptome and single-nucleus RNA sequence analyses, to explore the microbial mechanism of SARA occurrence and different degrees of inflammation. RESULTS: A total of 36 goats fed two diets with gradually increasing levels of rumen-degradable starch (RDS) were included in this study, and SARA goats fed 70% concentrate diets supplemented with whole corn (HGW-SARA) and SARA goats fed 70% concentrate diets supplemented with crushed corn (HGC-SARA) were identified. Moreover, 11 goats fed a control basal diet, named LGW-CON, were also included. Compared with those in the LGW-CON group, the rumen fermentation capacity was enhanced, accompanied by ruminal epithelial and systemic inflammation, in goats from HGW-SARA and HGC-SARA. Between them, HGC-SARA goats presented less inflammation. Notably, the ruminal inflammation-related pathways were increased only in the HGW-SARA group but not in the HGC-SARA group. Metagenomic analysis revealed that the β diversity of SARA goats was significantly different from that of LGW-CON goats. Ruminococcus significantly increased in both SARA groups, whereas Prevotella and Bacteroidales significantly decreased, which was accompanied by a decrease in cellulose and hemicellulose enzymes and an increase in lysozymes and lipopolysaccharide synthesis enzymes. Multi-omics analysis of the ruminal contents and tissues suggested that epithelial inflammation was caused by disturbed ruminal microbiome-induced Th17 cell differentiation and IL-17 signalling pathway activation. Comparative analyses between the HGW-SARA and HGC-SARA groups highlighted the importance of Selenomonas and Bifidobacterium, as well as bacterial tryptophan metabolism, in the production of 3-indoleacetic acid, which mitigated ruminal epithelial inflammation by modulating Th17 cells and inhibiting IL-17 signalling. Ruminal microbiota transplantation from HGW-SARA goats to healthy dairy goats and mice revealed the role of microbes in epithelial inflammation. Additionally, 3-indoleacetic acid supplementation reduced rumen inflammation and the IL-17 concentration in the serum, improved VFAs absorption, and enhanced milk production. CONCLUSIONS: This study unveiled that after SARA was induced by high-concentrate feeding, the rumen homeostasis was disrupted, and rumen fiber degradation capacity of dairy goats decreased, but the LPS synthesis capacity increased, and inflammation of the rumen epithelium was observed. However, the ruminal microbial species from the Bifidobacterium and Selenomonas genera and bacterial 3-indole acetic acid are pivotal in mitigating ruminal epithelial inflammation during SARA in dairy goats. This could potentially be attributed to the modulation of ruminal Th17 cell proportions and the inhibition of IL-17 signalling pathways. Video Abstract.
Rumen↗
Chronic inflammation in peritoneal dialysis: the search for the holy grail?
Mortality and morbidity in chronic kidney disease (CKD) patients are unacceptably high. The annual mortality rate due to cardiovascular disease (CVD) is approximately 9%, which, for the middle-aged person, is at least 10- to 20-fold higher than for the general population. Classic risk factors for CVD are highly prevalent in CKD patients, but they cannot fully account for the excessive rate of CVD in this population. Instead, it has become increasingly clear that nontraditional risk factors, such as systemic inflammation, may play a key role in the development of atherosclerosis. It is well established that inflammatory markers are very powerful predictors of high CVD morbidity and mortality not only in the general population, but particularly in CKD patients. Signs of a sustained low-grade inflammation, such as increased levels of C-reactive protein (CRP), are present in the majority of stage 5 CKD patients, even in patients in clinically stable condition, and they are also commonly observed after the initiation of dialysis therapy. Dialysis therapy--hemodialysis as well as peritoneal dialysis (PD)--may itself contribute to systemic inflammation. Local intraperitoneal inflammation can also occur in patients treated with PD. These local effects may result in a low-grade inflammation, caused by the bioincompatibility of conventional glucose-based dialysis fluids, to intense inflammation associated with peritonitis. Given these circumstances, it is reasonable to hypothesize that strategies aiming to reduce inflammation are potentially important and novel, and could serve to reduce CVD, thereby lowering morbidity and mortality in patients with CKD. In this review we provide information supporting the hypothesis that systemic inflammation is tightly linked to the most common complications of CKD patients, in particular those on PD, and that local inflammation in PD may contribute to various related complications. The aims of this review are to discuss the reasons that make inflammation an attractive target for intervention in CKD, the particular aspects of the inflammation-CVD axis during PD treatment that are likely involved, and possible means for the detection and management of chronic inflammation in PD patients.
C-Reactive Protein↗