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At least 19 recordsLinked to original sources
PubMedDate not supplied

A pilot study in the development of indices for predicting the clinical outcome of oral bone grafts.

PURPOSE: Bone grafting to repair osseous defects is widely used in dentistry, but little information on how to predict the clinical survival of grafted bone is currently available. As an initial step toward the establishment of formal criteria for predicting the clinical outcome of oral bone grafts, this pilot study sought to determine the relevance of adverse clinical and radiographic parameters as predictor variables for graft survival. MATERIALS AND METHODS: Eighty patients presenting with a variety of clinical conditions were treated with 83 oral bone grafts. Alloplastic, allogenic, and/or autogenous materials were used with or without barrier membranes. During follow-up appointments at 1 week, 1 month, 3 months, 6 months, 1 year, and 2 years after grafting, a series of clinical and radiographic parameters were used to evaluate the degree of graft integration. The data were then analyzed to determine the prediction accuracy of each variable in relation to the results of the graft. RESULTS: The findings of this clinical study suggest that the variables of (1) graft type, (2) inflammation, (3) infection, (4) fistula, (5) graft exposure, (6) pain, and (7) radiolucency were good indices for predicting graft survival, especially with cumulative data. DISCUSSION: The quality of the prognostic indices appeared to be good and should be further investigated for future applications. CONCLUSIONS: The cumulative index, with a sensitivity of 88.9% and a specificity of 93.8%, was the best predictor of clinical outcome. The 1-month and 3-month indices were similar.

Adolescent↗
PubMed2026

A distinct psoriasis-atopic dermatitis overlapping phenotype in adults with dual type 2 and type 3 immune features and favorable response to Janus kinase 1 inhibition.

BACKGROUND: Patients exhibiting overlapping histopathologic features of psoriasis (Pso) and atopic dermatitis (AD) present a diagnostic and therapeutic challenge. OBJECTIVES: To delineate the clinicopathological and immunologic portrait of psoriasis-atopic dermatitis overlapping (Pso-Ec) for integrated diagnosis and therapeutic decision-making. METHODS: We conducted a 2-center prospective study comparing 30 Pso-Ec patients with typical Pso and AD cohorts. Clinicopathological characteristics and immunologic profiling of lesional skin and peripheral blood were analyzed, and treatment courses were assessed. RESULTS: Pso-Ec patients (aged 13-72 years; mean age: 49.7 years) presented with ill-defined erythematous plaques with thin scales, excoriation, intense itching, and mixed psoriatic-eczematous histology. Immune profiling showed co-existence of helper T cell 2/cytotoxic T cell 2 and helper T cell 17/cytotoxic T cell 17 in skin and blood, with Janus kinase (JAK) 1 signal transducer and activator of transcription 2/6 signaling involvement. Responses to prior Pso-targeted (n = 18) and AD-targeted (n = 15) biologics were often inadequate. In contrast, JAK1 inhibitors achieved minimal disease activity (body surface area ≤ 2, numerical rating scale ≤1) during a median follow-up of 17 months. No progression to classic Pso or AD phenotypes was observed. LIMITATIONS: Sample size was limited and immunologic analyses were performed in a representative subset of patients. CONCLUSIONS: Pso-Ec represents a distinct, predominantly adult-onset phenotype driven by dual type 2 and type 3 inflammation, and JAK1 inhibitors appear as an effective option.

Humans↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMed1995

[The echographic assessment of the activity of the inflammatory process in patients with chronic acalculous cholecystitis in the choleretic test].

Ultrasonic investigations of the gallbladder in choleretic test were carried out in 186 patients with chronic acalculous cholecystitis (CAC): 47 with intensive, 76 with moderate and 31 with minimal exacerbation, 32 patients in remission and 36 control subjects. As shown by choleretic test, a reduction of latent period and gallbladder contraction duration, a decrease in discharged bile amount, bile discharge velocity, initial and final gallbladder volumes' ration and increased final gallbladder volume occurred in CAC patients. These changes were parallel to inflammation intensity. Three types of gallbladder contraction were revealed in choleretic test: a 3-phase contraction curve with the initial fast evacuation period, relaxation wave (enlarged gallbladder) and slow evacuation period (type 1); a 2-phase curve with fast and slow evacuation (type 2); a monophasic curve with slow evacuation (type 3). In the patients studied type 1 prevailed, while type 3 was not observed in the controls. With increasing inflammation activity in CAC patients a type-1 contraction frequency declined and disappeared in active exacerbation, whereas type 2 and especially type 3 contractions became more frequent.

Adolescent↗
PubMed2000

Impairment of Ca(2+) mobilization in circular muscle cells of the inflamed colon.

This study investigated whether inflammation modulates the mobilization of Ca(2+) in canine colonic circular muscle cells. The contractile response of single cells from the inflamed colon was significantly suppressed in response to ACh, KCl, and BAY K8644. Methoxyverapamil and reduction in extracellular Ca(2+) concentration dose-dependently blocked the response in both normal and inflamed cells. The increase in intracellular Ca(2+) concentration in response to ACh and KCl was significantly reduced in the inflamed cells. However, Ca(2+) efflux from the ryanodine- and inositol 1,4, 5-trisphosphate (IP(3))-sensitive stores, as well as the decrease of cell length in response to ryanodine and IP(3), were not affected. Heparin significantly blocked Ca(2+) efflux and contraction in response to ACh in both conditions. ACh-stimulated accumulation of IP(3) and the binding of [(3)H]ryanodine to its receptors were not altered by inflammation. Ruthenium red partially inhibited the response to ACh in normal and inflamed states. We conclude that the canine colonic circular muscle cells utilize Ca(2+) influx through L-type channels as well as Ca(2+) release from the ryanodine- and IP(3)-sensitive stores to contract. Inflammation impairs Ca(2+) influx through L-type channels, but it may not affect intracellular Ca(2+) release. The impairment of Ca(2+) influx may contribute to the suppression of circular muscle contractility in the inflamed state.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2005

Hepatic histopathology of patients with morbid obesity submitted to gastric bypass.

BACKGROUND: The authors analyze and describe the hepatic histopathology of patients with morbid obesity submitted to gastric bypass. METHODS: A liver biopsy was performed in 112 patients at the beginning of gastric bypass, and clinical data (gender, age, BMI and associated diseases) were obtained from the patient records. RESULTS: Among the patients, 74.1% (n=83) were females and 25.9% (n=29) were males, age 39.59+/-10.12 years, with BMI 48.79+/-7.54. Regarding the diseases associated with morbid obesity, arterial hypertension was observed in 67.9% (n=76) of the patients, joint diseases in 55.4% (n=62), dyslipidemia in 40.2% (n=45), and diabetes type 2 in 27.7% (n=31). 111 patients (99.1%) showed different types of non-alcoholic fatty liver disease (NAFLD) (types 1, 2, 3 and 4), with types 3 and 4 accounting for 57.7% (n=64). A significant association was observed between NAFLD type 4 and diabetes type 2 (P=0.018). The presence of glycogen nuclei was significantly correlated with steatosis (P=0.000), lobular inflammation (P=0.019) and perisinusoidal fibrosis (P=0.000). CONCLUSION: 1) Liver biopsy taken at gastric bypass reveals different types of NAFLD; 2) Diabetes type 2 is associated with NAFLD type 4; 3) Glycogen nuclei are correlated with steatosis, lobular inflammation and perisinusoidal fibrosis; 4) Steatosis represents the basic injury in NAFLD and is associated with hepato-cellular ballooning. 5) In view of the frequency of hepatic alterations, a biopsy should be part of the surgical protocol of morbid obesity, this method being the only one able to determine the presence of lesions and to stage fibrosis.

Adult↗
PubMed2006

Monocytes from type 2 diabetic patients have a pro-inflammatory profile. 1,25-Dihydroxyvitamin D(3) works as anti-inflammatory.

The exact factors contributing to the pathogenesis of type 2 diabetes remain elusive. Lately, it was suggested that inflammation and activation of the innate immune system could be linked to type 2 diabetes pathogenesis and also to the development of common diabetic complications, mainly atherosclerosis. The aim of this study was to investigate the role of monocytes in this sub-clinical inflammatory state and test 1,25-dihydroxyvitamin D(3), the active form of Vitamin D, as an anti-inflammatory agent. For this purpose, monocytes from type 2 diabetic patients were compared to monocytes from healthy controls and type 1 diabetic patients. The expression profile of inflammatory markers in freshly isolated and immune-stimulated monocytes was measured by quantitative real-time RT-PCR. Type 2 diabetic patients showed significantly higher expression levels of TNF-alpha, IL-6, IL-1, IL-8, COX-2, ICAM-1 and B7-1 compared to controls and type 1 diabetic patients. 1,25-Dihydroxyvitamin D(3) was able to down-regulate the expression of TNF-alpha, IL-6, IL-1, and IL-8, confirming its immunomodulatory properties. From these data we concluded that monocytes from type 2 diabetic patients have a pro-inflammatory profile. In addition, 1,25-dihydroxyvitamin D(3) was able to modulate inflammation in these monocytes.

Adolescent↗
PubMed2005

[Metabolic syndrome: which definition for what treatment(s)?].

Metabolic syndrome is asymptomatic and results from the increasing prevalence of obesity. Although several definitions exist and complicate its diagnosis, metabolic syndrome is characterized by the clustering of moderate troubles of glucose, lipid metabolism, body weight, hypertension and vascular inflammation ; the synergy between 3 of them triggers type 2 diabetes, atherosclerosis and associated clinical events. Whatever the age but particularly in adolescence, the prevalence of metabolic syndrome is high ; beyond lifestyle interventions, the available treatments address essentially a single risk factor and an unmet medical need persists. The reduction of cardiovascular events in secondary prevention has been demonstrated for some antidiabetic, hypolipidemic and antihypertensive agents but any difference in efficacy between populations with and without metabolic syndrome has yet to be established. The approval of metabolic syndrome as a specific therapeutic target would need the characterization of its pathogenic mechanism, a clearer guidance for definition and diagnosis, and the clinical proof of concept of a novel molecule displaying multifactorial impacts. Some new mechanistic approaches are discussed and may represent a breakthrough particularly if positive results of Field and Proactive clinical studies related to PPARs are disclosed soon.

Humans↗
PubMedDate not supplied

Using Tc-99m DMSA renal cortex scan to detect renal damage in women with type 2 diabetes.

Women with diabetes mellitus (DM) have urinary tract infection (UTI) more often than women without DM. It is unknown, however, what the prevalence and type of renal damage due to UTI is in these women. Therefore, in this study, we compared type 2 DM women with or without UTI history for the prevalence and type of renal damage by technetium-99m dimercapto-succinic acid (Tc-99m DMSA) renal scan. A total of 128 type 2 DM women with or without UTI history received Tc-99m DMSA renal scan were included in this study. The patients were separated into three groups: (1) 43 patients without UTI history, (2) 42 patients with only lower UTI (cystitis) history and (3) 43 patients with upper UTI (pyelonephritis) history. The renal scan findings were separated into three types: (A) normal, (B) inflammation and (C) scar. The 31.9% (50/128) of type 2 DM patients had renal damages. Group 1 patients had a significantly lower prevalence of renal damages including inflammation and scar as compared to Groups 2 and 3 patients. In addition, the prevalence of renal damage was significantly higher in Group 3 than in Group 2 patients. Renal scars only were visualized in Group 3 patients. However, other clinical data were not statistically different among the three group patients. Type 2 DM women with UTI history, especially if they had upper UTI have a significantly higher prevalence of renal damage than in those without UTI.

Biological Transport↗
PubMed2003

Autopsy-based assessment of extent and type of osteomyelitis in advanced-grade sacral decubitus ulcers: a histopathologic study.

CONTEXT: Decubitus ulcers constitute a serious medical problem, often encountered in association with hospitalization or institutionalization in senior citizens' or nursing homes. Potentially life-threatening sepsis has been reported to originate not only from soft tissue infection, but also from osteomyelitis as a complication of involvement of bone tissue in decubitus ulcers. OBJECTIVE: To assess the histopathology of osseous structures involved in grade IV decubitus ulcers. DESIGN: Autopsy-based histopathologic assessment of the presence and extent of osteomyelitis on os sacrum specimens from 28 deceased individuals with grade IV sacral decubitus ulcers using an undecalcified preparation following plastic embedding (staining with Goldner, Kossa modification, toluidine blue, and Giemsa). RESULTS: The histologic findings were classified in 4 types of pathomorphologic changes: type 1, decubitus ulcer confined to soft tissue, no inflammation (n = 7); type 2, decubitus ulcer involving bone, no inflammation (n = 7); type 3, decubitus ulcer involving bone, inflammation of soft tissue, no osteomyelitis (n = 1); and type 4, decubitus ulcer involving bone, presence of osteomyelitis (n = 13). Type 4 changes are further described as follows: type 4a, chronic osteomyelitis alone (n = 6); and type 4b, chronic and acute osteomyelitic changes (n = 7). More than half of the cases (n = 15) showed no inflammatory reaction within the medullary cavity (types 1-3). In all cases with osteomyelitis, inflammation was exclusively confined to the superficial parts of the os sacrum. Chronic osteomyelitis was seen in all cases in which osteomyelitis was present. In addition, mild acute osteomyelitic changes were observed in 7 cases. Severe liquefying osteomyelitis affecting deeper layers of the os sacrum was not found. Sepsis was present in 2 cases; in one of these cases, the decubitus ulcer was considered a possible source of infection. CONCLUSIONS: Our results provide evidence that in cases of grade IV decubitus ulcers, the macroscopic aspect and clinical imaging techniques may lead to an overestimation of the extent of osseous involvement. We suggest that the investigation of bone biopsies is not necessary in a considerable proportion of cases of grade IV decubitus ulcers in patients without sepsis, as the minor osseous alterations are of little consequence when establishing a therapeutic approach.

Aged↗
PubMed2004

Inhibition of L-type Cav1.2 Ca2+ channels by 2,(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002) and 2-[1-(3-dimethyl-aminopropyl)-5-methoxyindol-3-yl]-3-(1H-indol-3-yl) maleimide (Go6983).

Phosphatidylinositol 3-kinase (PI3-K) is involved in physiological processes of cellular proliferation and inflammation and, as postulated recently, in the regulation of L-type Ca(2+) channels. The latter conclusion arose in part from the inhibitory action of the compound 2,(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002), which has been established as a selective PI3-K inhibitor (IC(50) = 1.4 microM). Herein we show, however, that LY294002 and an inhibitor of protein kinase C (PKC), 2-[1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl]-3-(1H-indol-3-yl) maleimide (Go6983), act as direct Ca(2+)-channel inhibitors, with IC(50) values of approximately 20 and 10 microM, respectively. Because both drugs are commonly used at concentrations of approximately 10 microM or higher, the interpretation of such experiments is questionable with respect to a regulatory action of PI3-K or PKC on L-type Ca(2+) channels.

Animals↗
PubMed1981

[Morphological manifestations of the immune reactions in stomach cancer and their relation to the histological structure of the tumor].

The morphology of immune response in tumor tissue was studied in the resected material obtained from 244 patients with stomach cancer. In nearly 80% of cases of carcinoma, the following five morphological types were observed: (1) acute inflammation (immediate--onset hyperergy); (2) time--delayed hyperergy; (3) plasmocytic--eosinophilic cellular infiltration with tumor mucination; (4) chronic granulomatous inflammation and (5) lymphadenoid and fibrose tissue envelope of tumor. There established a relationship between the type and degree of immune reactions and the histology of tumor. Progressing, regressing and stable reactions should be distinguished. Tumor regression and immune response were observed in foci; however, complete resolution was registered in 2.5% of cases only.

Antigen-Antibody Reactions↗
PubMed1992

Pathological studies on Takayasu arteritis.

Takayasu arteritis is a primary inflammatory disease of elastic arteries such as the aorta, its larger branches and the pulmonary artery trunk. According to our recent statistical survey of autopsy cases in Japan, the frequency of the disease in all autopsy cases was approximately 0.033% and the sex ratio was 1:4.5. The most frequent ages of the onset were 20-30 years, those of the death were 40-50 years. The latter was delayed about 20 years in comparison with a previous report. In the recent cases, the vascular lesions widely expanded. Luminal dilatation and aneurysm formation also increased in frequency, their ratio being approximately 57%. In the autopsy cases, the following active lesions were observed: (1) acute exudative inflammation (including suppuration), (2) chronic non-specific productive inflammation and (3) various types of granulomatous inflammation. These findings suggest that many triggers may play a role in the morphogenesis of Takayasu arteritis. The inflammatory lesions are produced in the media and adventitia through the vasa vasorum, and terminate in a diffuse or nodular fibrosis. New active lesions are often observed near the old fibrotic ones. This suggests that Takayasu arteritis may be a progressive disease. Intimal thickening of the peripheral branches from the affected arteries is very often observed. In consequence, secondary ischemic lesions are formed in various organs, especially the heart, brain and kidneys.

Adolescent↗
PubMed2006

Treatment of allergic airway inflammation and hyperresponsiveness by imiquimod modulating transcription factors T-bet and GATA-3.

BACKGROUND: Imiquimod is an imidazoquinoline, which class of compounds are known to have antiviral and antitumoural properties. In recent studies, it was shown that imiquimod modulates the T helper cell type Th1/Th2 response by inducing the production of Th1 cytokines like IFN-gamma, and by inhibiting the Th2 cytokines like interleukin (IL)-4. Several investigators have shown that T-bet and GATA-3 are master Th1 and Th2 regulatory transcription factors. This study investigated whether imiquimod treatment inhibited airway inflammation by modulating transcription factors T-bet and GATA-3. METHODS: Thirty-six male SD rats were randomly divided into a control group, an asthmatic group, and an imiquimod group, which was exposed to an aerosol of 0.15% imiquimod. Twenty-four hours after the last ovalbumin (OVA) challenge, airway responsiveness was measured and changes in airway histology were observed. The concentrations of IL-4, IL-5 and IFN-gamma in bronchoalveolar lavage fluid (BALF) and serum were measured by enzyme linked immunosorbent assay (ELISA). The mRNA expressions of IL-4, IL-5, IFN-gamma, T-bet and GATA-3 in lung and in CD4(+) T cells were determined by reverse transcription polymerase chain reaction (RT-PCR). The protein expressions of T-bet and GATA-3 were measured by Western blot. RESULTS: It was demonstrated that imiquimod 1) attenuated OVA induced airway inflammation; 2) diminished the degree of airway hyperresponsiveness (AHR); 3) decreased the Th2 type cytokines and increased Th1 type cytokines mRNA and protein levels; 4) modulated the Th1/Th2 reaction by inhibiting GATA-3 production and increasing T-bet production. CONCLUSION: Imiquimod treatment inhibits OVA induced airway inflammation by modulating key master switches GATA-3 and T-bet that result in committing T helper cells to a Th1 phenotype.

Administration, Inhalation↗
PubMed2001

Antichemokine immunotherapy for allergic diseases.

Chemokines have emerged as critical regulators of leukocyte function and as such represent attractive new targets for the therapy of allergic diseases. Recent studies have revealed important roles for the chemokine family in both the afferent and efferent limbs of the immune system, orchestrating and integrating innate and acquired immune responses. A subset of chemokines including eotaxin-1 (also called CCL11), eotaxin-2 (CCL24), eotaxin-3 (CCL26), MCP (monocyte chemoattractant protein)-3 (CCL7), MCP (monocyte chemoattractant protein)-4 (CCL13), TARC (thymus- and activation-regulated chemokine) (CCL17), and MDC (macrophage-derived chemokine) (CCL22) are highly expressed in allergic inflammation and are regulated by T helper type 2 cytokines. Receptors for these chemokines, including CCR3 (CC chemokine receptor 3), CCR4 (CC chemokine receptor 4) and CCR8 (CC chemokine receptor 8) are expressed on key leukocytes associated with allergic inflammation, such as T helper type 2 cells, eosinophils, mast cells and basophils, establishing a subset of chemokine/chemokine receptors potentially important in allergic inflammation. Recent data using inhibitory antibodies and chemokine antagonists support the concept that interfering with this subset of chemokines and their receptors represents a new approach to allergy immunotherapy.

Chemokines↗
PubMed2004

Vitamin D receptor-deficient mice fail to develop experimental allergic asthma.

The active metabolite of vitamin D (1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3))) is known to modulate the immune response in Th1 cell-directed diseases. To investigate the role of vitamin D in Th2 cell-directed diseases, experimental allergic asthma was induced in vitamin D receptor (VDR) knockout and in wild-type (WT) mice. As expected, WT mice developed symptoms of airway inflammation with an influx of eosinophils, elevated Th2 cytokine levels, mucous production, and airway hyperresponsiveness. The administration of 1,25(OH)(2)D(3) had no effect on asthma severity. The only discernable effect of 1,25(OH)(2)D(3) on experimental allergic asthma in WT mice was an increased expression of two Th2-related genes (soluble CD23 and GATA-3) in lungs of BALB/c mice exposed to Ag through the nasal route only. By contrast, asthma-induced VDR knockout mice failed to develop airway inflammation, eosinophilia, or airway hyperresponsiveness, despite high IgE concentrations and elevated Th2 cytokines. The data suggest that although 1,25(OH)(2)D(3) induced these Th2-type genes, the treatment failed to have any affect on experimental asthma severity. However, VDR-deficient mice failed to develop experimental allergic asthma, suggesting an important role for the vitamin D endocrine system in the generation of Th2-driven inflammation in the lung.

Animals↗
PubMed1983

Experimental partial ureteric obstruction in newborn rats. IV. Do the morphological effects progress continuously?

Partial obstruction of the ureter was created in newborn rats, and its effects were studied after 1, 2, 3, 6 and 9 weeks--that is, until adult age. Within 1 week, a considerable hydronephrosis had appeared. Within 2 weeks, parenchymal weight was found slightly reduced (8 per cent) on the obstructed side, and, within 3 weeks, equivalently increased on the contralateral, intact side. After these points in time, there was no further deterioration. Histological examination revealed marked deformation of the papilla and minor foci of degeneration and inflammation within 1 to 2 weeks which tended to become chronic in type after 3 to 9 weeks. Arterial hypertension was not noted. Thus, the effects of partial ureteric obstruction on the renal parenchyma are 1) discrete, 2) not in proportion to the degree of hydronephrosis, 3) fully compensated by contralateral hypertrophy and 4), after reaching an early maximum, not increasing with time.

Aging↗