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At least 55 records · Page 3Linked to original sources
PubMed1979

The early development of white adipose tissue. Effects of litter size on the lipoprotein lipase activity of four adipose-tissue depots, serum immunoreactive insulin and tissue cellularity during the first four weeks of life in the rat.

1. Newborn rats were reared in litters of either four or sixteen individuals. The animals from the small litters gained body weight more rapidly than those from large litters during the first 29 days of postnatal life studied. 2. The relative weights of the perigenital, perirenal, subcutaneous and intramuscular white-adipose-tissue sites in the animals from small litters indicated their relative obesity compared with controls. 3. The adipose depots from animals reared in small litters had a greater proportion of lipid present, by weight, and had a greater number of larger fat-cells present in them compared with the depots of animals reared in large litters. 4. Compared with both normal-sized litter controls and animals reared in sixteens, during the period of study the animals from small litters were hypertriacylglycerolaemic but normocholesterolaemic. 5. During suckling the blood glucose concentrations of animals reared in fours were increased, as were the concentrations of circulating immunoreactive insulin. 6. During the 29 days of life studied, in general, the lipoprotein lipase activity of adipose depots from animals reared in fours was greater than for animals in large litters when expressed as mumol of nonesterified fatty acid released from the substrate/h per g fresh weight of tissue, per depot, or per million fat-cells, but were similar per cm(2) of fat-cell surface area. 7. The previously noted [Cryer & Jones (1978) Biochem. J.172, 319-325] pattern of mid-suckling elevation, late-suckling decline and post-weaning increase in the lipoprotein lipase activity of the four white-adipose depots studied was not obliterated by the nutritional manipulations employed. 8. The relation of the enzyme-activity changes and their hormonal stimuli to triacylglycerol accumulation in fat-cells of animals from large and small litters is discussed in relation to the possible significance they may have to our understanding of neonatally induced obesity.

Adipose Tissue↗
PubMed1989

[A comparative study of the biological behavior of gastric cancer from the view of the amount of connective tissue in the cancerous tissue--a correlation between the amount of connective tissue and the metastatic pattern].

Differences between advanced gastric cancer of the medullary type (med.: 138 cases) and the scirrhous type (sci: 164 cases) with regard to the amount of connective tissue that was cancerous have been studied clinicopathologically. A correlation was found between med and liver metastasis, and sci and peritoneal dissemination in metastatic types, whereas no correlation was observed in other factors except between med and a localized type, sci and infiltrating type in gross type. The study of tumorigenicity in nude mice showed remarkable difference between med (86.7%) and sci. (0%). These results indicate that there is definite relationship between the amount of connective tissue and the biological behavior of a gastric cancer.

Adenocarcinoma, Scirrhous↗
PubMed1989

[Studies on regulation of the function of thermogenic tissue, brown adipose tissue (BAT) by means of tissue culture method].

In order to clarify the regulatory mechanism of BAT function, the effects of noradrenaline (NA) (6mM), insulin (I) (40nM), glucagon (G) (400nM) and nerve growth factor (NGF) (2-10nM), alone or in combination, were investigated directly in BAT from neonatal rats (ca. 3 days old), cultured in 10% fetal bovine serum-medium 199 in 95% air-5% CO2 gas phase at 33 degrees C for 1 to 2 weeks. I stimulated lipid accumulation and enlarged outgrown cell size, but mitochondria in the cells of tissue block were smaller and their cristae less distinct. I + G enlarged nucleus and cytoplasm, and suppressed the lipid accumulation induced by I, but mitochondria in the cells of tissue block were larger and their cristae became more prominent than those of I-added cells. G induced the similar changes to those by I + G. I + NA also induced the similar effects to those by I + G, but their mitochondria size did not differ from that of I-added cells. NGF caused the similar effects of those by G, inducing the development of mitochondria, rough endoplasmic reticulum and Golgi complex. These results suggest that multiple factors such as NA, I, G and NGF regulate differentiation and functional development of BAT.

Adipose Tissue↗
PubMed1977

The metabolism of prostaglandins F2alpha and E2 by non-pregnant porcine endometrial and luteal tissue and early pregnant porcine endometrial tissue, luteal tissue and conceptuses in vitro.

Slices of porcine endometrium and corpus luteum from both early pregnant and non-pregnant sows and conceptuses from early pregnant sows were incubated with radioactive PGF2alpha and PGE2 and the degree of metabolism of the prostaglandins measured. Prostaglandins and a metabolites were separated by TLC, radioactive bands located with a Panax scanner and the radioactivity measured in a scintillation counter. Endometrial and luteal tissue from non-pregnant sows gave no significant metabolism at any stage of the oestrous cycle, and while similar tissue from pregnant sows metabolised both prostaglandins slightly, only the conceptuses gave any significant metabolism. The possible physiological significance of these results is discussed.

Animals↗
PubMed2003

Probing the interface between factor Xa and tissue factor in the quaternary complex tissue factor-factor VIIa-factor Xa-tissue factor pathway inhibitor.

Blood coagulation is triggered by the formation of a complex between factor VIIa (FVIIa) and its cofactor, tissue factor (TF). TF-FVIIa is inhibited by tissue factor pathway inhibitor (TFPI) in two steps: first TFPI is bound to the active site of factor Xa (FXa), and subsequently FXa-TFPI exerts feedback inhibition of TF-FVIIa. The FXa-dependent inhibition of TF-FVIIa activity by TFPI leads to formation of the quaternary complex TF-FVIIa-FXa-TFPI. We used site-directed fluorescence probing to map part of the region of soluble TF (sTF) that interacts with FXa in sTF-FVIIa-FXa-TFPI. We found that the C-terminal region of sTF, including positions 163, 166, 200 and 201, is involved in binding to FXa in the complex, and FXa, most likely via its Gla domain, is also in contact with the Gla domain of FVIIa in this part of the binding region. Furthermore, a region that includes the N-terminal part of the TF2 domain and the C-terminal part of the TF1 domain, i.e. the residues 104 and 197, participates in the interaction with FXa in the quaternary complex. Moreover, comparisons of the interaction areas between sTF and FX(a) in the quaternary complex sTF-FVIIa-FXa-TFPI and in the ternary complexes sTF-FVII-FXa or sTF-FVIIa-FX demonstrated large similarities.

Amino Acid Substitution↗
PubMed2000

Changes of plasma tissue factor and tissue factor pathway inhibitor antigen levels and induction of tissue factor expression on the monocytes in coronary artery disease.

BACKGROUND: Several studies have shown that thrombosis and inflammation play an important role in the pathogenesis of coronary artery disease (CAD). Tissue factor (TF) is responsible for the thrombogenicity of the atherosclerotic plaque and plays a key in triggering thrombin generation. The aim of this study was to assess the levels of TF and tissue factor pathway inhibitor (TFPI) in patients with angiographically documented CAD and also to evaluate TF induction on monocytes in vitro in the presence of these plasmas from patients with CAD. METHODS: Plasma antigen levels of soluble TF and TFPI were measured in 65 CAD patients and 22 healthy controls. Surface TF expression on monocytes from a healthy donor treated with plasma samples was evaluated by flow cytometry with a direct double-color immunofluorescence technique. RESULTS: Significantly elevated levels of both TF and TFPI were found in CAD patients compared with healthy controls (303.6 +/- 134.1 vs. 187.3 +/- 108.7 pg/ml, p < 0.05; 85.2 +/- 48.6 vs. 65.0 +/- 29.0 ng/ml, p < 0.05). By flow cytometry, monocytes from a healthy donor displayed higher TF antigen expression when incubated in the presence of CAD plasmas than in control plasmas (34.6 +/- 10.7 vs. 23.2 +/- 10.2%, p < 0.05). CONCLUSIONS: The high levels of circulating TF are present in CAD, which were not sufficiently inhibited by the elevated TFPI plasma levels. Although the source of circulating TF is unclear, TF induction of monocytes by plasma from CAD patients may contribute to the hypercoagulable state.

Adult↗
PubMed1986

Expression of mouse beta 2-microglobulin in frozen and formaldehyde-fixed central nervous tissues: comparison of tissue behind the blood-brain barrier and tissue in a barrier-free region.

Previous work indicates that the weak expression in neural tissues of beta 2-microglobulin (beta 2-m) and major histocompatibility complex (MHC) class I gene products can be increased experimentally. Physiologic conditions in which greater neural MHC expression occurs are not well defined. Here we have asked whether protection from blood-borne antigens afforded by the blood-brain barrier is related to the lack of MHC expression. A rabbit antiserum raised against purified mouse beta 2-m was used in an immunocytochemical assay. The serum reacted strongly with lymphoid tissues and was inhibited by purified beta 2-m. No beta 2-m was detected in neurons or glia in any brain area examined. A barrier-free region, the area postrema, showed the same lack of neural cell staining. Blood vessel walls in the same sections were beta 2-m+. It is unlikely that these staining patterns are due to cell type-specific beta 2-m degradation, since frozen and formaldehyde-perfused, paraffin-embedded preparations gave similar results. Failure to detect beta 2-m in the area postrema suggests that passive exposure to environmental antigens, immunomodulators, or immunocompetent cells is not sufficient to induce neural class I expression. Rather, if increased expression of beta 2-m and class I occurs in vivo, additional stimulus is required.

Animals↗
PubMed1991

The purification of tissue inhibitor of metalloproteinases-2 from its 72 kDa progelatinase complex. Demonstration of the biochemical similarities of tissue inhibitor of metalloproteinases-2 and tissue inhibitor of metalloproteinases-1.

Human gingival fibroblasts in culture were shown to secrete a 72 kDa progelatinase, of which a proportion in the medium was found to be complexed with tissue inhibitor of metalloproteinases-2 (TIMP-2). A purification procedure was devised to purify free enzyme and inhibitor. We also describe the purification of both 95 kDa progelatinase bound to TIMP-1 and free 95 kDa progelatinase from the medium of U937 cells. A polyclonal antiserum to TIMP-2 was prepared and it was shown that TIMP-1 and TIMP-2 are antigenically distinct. The ability to form stable complexes and the relative inhibitory activities of TIMP-1 and TIMP-2 towards 95 kDa and 72 kDa gelatinases, collagenase, stromelysins 1 and 2 and punctuated metalloproteinase were determined; only minor differences were found. Complex-formation between TIMP-2 and 72 kDa progelatinase was demonstrated not to reduce the metalloproteinase-inhibitory activity of TIMP-2, a finding that led to the characterization of high-molecular-mass TIMP activity. Competition experiments between progelatinases and active gelatinases for TIMPs indicated that the affinity of TIMPs for progelatinases is weaker than that for active gelatinases. In a study of the effects of TIMP-1 and TIMP-2 on progelatinase self-cleavage we found that both TIMP-1 and TIMP-2 inhibit the conversion of 95 kDa and 72 kDa progelatinases and prostromelysin into lower-molecular-mass forms. TIMP capable of complexing with progelatinase was shown to be no more efficient an inhibitor of gelatinase self-cleavage than TIMP not able to complex with progelatinase.

Amino Acid Sequence↗
PubMed1996

Early undifferentiated connective tissue disease. IV.Musculoskeletal manifestations in a large cohort of patients with undifferentiated connective tissue diseases compared with cohorts of patients with well-established connective tissue diseases: followup analyses in patients with unexplained polyarthritis and patients with rheumatoid arthritis at baseline.

OBJECTIVES: To examine the musculoskeletal manifestations in a large cohort of patients (n = 410) diagnosed with either a well-established connective tissue disease (CTD) (n = 197) or an early undifferentiated CTD (n = 213) with a symptom duration of <1 year. This study was aimed at determining the predictive value of demographic, clinical, and laboratory features on outcome in patients with unexplained polyarthritis (UPA) (from the early undifferentiated CTD cohort; n = 67) or rheumatoid arthritis (RA) (from the well-established CTD cohort; n = 57), over a 5-year followup period. METHODS: Patients from both cohorts were assessed at years 1, 3, and 5. At the study visits, clinical data were collected in a standardized manner, and sera were obtained and stored. A priori criteria were established for patient ascertainment and diagnosis over the duration of the study. Standard statistics were used for comparisons of baseline characteristics in patients diagnosed as having systemic lupus erythematosus, RA, undifferentiated CTD, and UPA at entry into the cohorts. Baseline features in patients with UPA were examined according to the different subsequent outcomes (RA, CTD, or undifferentiated CTD, remission [nonpersistent], or persistent or active UPA). Baseline features in patients with RA whose disease remained active versus those in whom remission was attained were also examined. Two multivariable analyses, classification trees and polychotomous logistic regression, were performed to predict disease outcomes over time. RESULTS: The overall rate of ascertainment for the 410 patients ranged from 90 % at year 1 to 71 % at year 5. Patients with established CTDs showed a tendency for more stable diagnoses than those with early undifferentiated CTDs (90-100% versus 45-70%). Consistent baseline predictors of persistent active disease among patients with RA, in both univariate and multivariable analyses, were higher joint counts for pain and tenderness and higher erythrocyte sedimentation rate (ESR). In approximately 20% of patients who were classified as having RA when they originally entered the cohort, the disease was in remission at 5 years. Twenty percent of the patients originally classified as having UPA developed RA over the duration of the study. These patients tended to be older and to have swelling of small joints at baseline. However, a consistent pattern of predictive variables could not be identified in the multivariable analyses, other than at year 1 (higher small joint counts for swelling and higher ESR). CONCLUSION: Baseline features (joint counts, and ESR) among RA patients were variously predictive of persistently active disease at years 1-5. Consistent baseline predictors of outcome among patients with UPA only emerged at year 1. Remission occurred in approximately 20% of RA patients, whereas a similar percentage of patients with UPA developed RA. These findings have implications with regard to treatment decisions in patients with early RA and/or UPA.

Adult↗
PubMed1991

Early undifferentiated connective tissue disease. I. Early clinical manifestation in a large cohort of patients with undifferentiated connective tissue diseases compared with cohorts of well established connective tissue disease.

We identified a cohort of 410 patients with connective tissue disorders (CTD) of less than or equal to 1 year duration among the participating clinics of the Cooperative Systematic Studies of the Rheumatic Diseases Program. Fifty-seven had rheumatic arthritis (RA), 57 systemic lupus erythematosus, 37 poly/dermatomyositis, 46 scleroderma, and 213 early undifferentiated CTD, including patients with Raynaud's phenomenon, unexplained polyarthritis or at least 3 CTD manifestations such as rashes, myalgias, etc. Baseline clinical data are now being reported. The followup of these patients may prove to be valuable in understanding these diseases. To our knowledge no similar cohort of patients is available for further investigation.

Adolescent↗
PubMed2004

Effects of crosslinking degree of an acellular biological tissue on its tissue regeneration pattern.

It was reported that acellular biological tissues can provide a natural microenvironment for host cell migration and may be used as a scaffold for tissue regeneration. To reduce antigenicity, biological tissues have to be fixed with a crosslinking agent before implantation. As a tissue-engineering scaffold, it is speculated that the crosslinking degree of an acellular tissue may affect its tissue regeneration pattern. In the study, a cell extraction process was employed to remove the cellular components from bovine pericardia. The acellular tissues then were fixed with genipin at various known concentrations to obtain varying degrees of crosslinking. It was shown in the in vitro degradation study that after fixing with genipin, the resistance against enzymatic degradation of the acellular tissue increased significantly with increasing its crosslinking degree. In the in vivo subcutaneous study, it was found that cells (inflammatory cells, fibroblasts, endothelial cells, and red blood cells) were able to infiltrate into acellular tissues. Generally, the depth of cell infiltration into the acellular tissue decreased with increasing its crosslinking degree. Infiltration of inflammatory cells was accompanied by degradation of the acellular tissue. Due to early degradation, no tissue regeneration was observed within fresh (without crosslinking) and the 30%-degree-crosslinking acellular tissues. This is because the scaffolds provided by these two samples were already completely degraded before the infiltrated cells began to secrete their own extracellular matrix. In contrast, tissue regeneration (fibroblasts, neo-collagen fibrils, and neo-capillaries) was observed for the 60%- and 95%-degree-crosslinking acellular tissues by the histological examination, immunohistological staining, transmission electron microscopy, and denaturation temperature measurement. The 95%-degree-crosslinking acellular tissue was more resistant against enzymatic degradation than its 60%-degree-crosslinking counterpart. Consequently, tissue regeneration was limited in the outer layer of the 95%-degree-crosslinking acellular tissue throughout the entire course of the study (1-year postoperatively), while tissue regeneration was observed within the entire sample for the 60%-degree-crosslinking acellular tissue. In conclusion, the crosslinking degree determines the degradation rate of the acellular tissue and its tissue regeneration pattern.

Animals↗
PubMed2000

Physical properties of the mitral valve tissue assessed by tissue sound speed in cardiac amyloidosis: relationship to the severity of mitral regurgitation.

Cardiac amyloidosis has been documented to show mitral regurgitation (MR) and a thickened mitral valve (MV) due to amyloid deposits. However, the changes in the physical properties of the thickened MV tissue in cardiac amyloidosis, which may be a causative factor of the MR, have not been described. Physical properties of the tissue, which are expressed by the elastic bulk modulus, can be evaluated by tissue sound speed. If biological tissue is assumed to be fluid-like, the tissue sound speed may be given by c= square root of K/rho, where c is the tissue sound speed, K is the elastic bulk modulus, and rho is the density. A reduction in tissue sound speed indicates a reduction in the elastic bulk modulus of the tissue, assuming that there is little change in rho. This suggests that the tissue is less elastic. The purpose of this study was to assess the physical properties of MV tissue by evaluating the sound speed of the MV tissue in cardiac amyloidosis. MV specimens were obtained at autopsy from 20 control adults without cardiovascular diseases and from 20 patients with cardiac amyloidosis. An acoustic microscope operating at 450 MHz was used to measure the tissue sound speed in the tip and basal portions of the MV tissue. The density of MV tissue was measured by microgravimetry. The severity of the MR had been evaluated by Doppler echocardiography before death, and it was compared with the tissue sound speed measured after death. In cardiac amyloidosis showing mild MR, the tissue sound speed of the MV in the tip portion (1605 +/- 19 m/s) and in the basal portion (1791 +/- 64 m/s) were lower than the corresponding values in control subjects (1637 +/- 42 m/s and 1851 +/- 62 m/s). However, these differences were not statistically significant. In cardiac amyloidosis showing moderate MR, the tissue sound speed of MV in the tip portion (1563 +/- 17 m/s) and in the basal portion (1654 +/- 59 m/s) were significantly lower than the corresponding values in the control subjects (p < 0.001) and the patients with mild MR (p < 0.05). No significant differences were observed in the density of MV tissue among the three groups. Therefore, the low value of the MV tissue sound speed in patients with cardiac amyloidosis indicated a reduced elastic bulk modulus, suggesting the less elasticity of the MV tissue. Furthermore, the patients with moderate MR demonstrated the greater reduction in the tissue sound speed than the patients with mild MR. The data suggest that the changes in physical properties of the MV tissue may be one of the causes of MR in cardiac amyloidosis.

Acoustics↗
PubMed1997

Determination of silicon in breast and capsular tissue from patients with breast implants performed by inductively coupled plasma emission spectroscopy. Comparison with tissue histology.

A method for analysis of silicon in tissue was developed to determine silicon content in breast parenchymal and periprosthetic capsular tissues of patients with silicone or saline implants and to compare levels in tissues from normal (nonaugmented) breasts. It is of interest to determine whether increased silicon content in tissues can be associated with morbidity in patients who have received silicone implants. This manuscript addresses the issues involved in analysis of breast tissue samples for silicon and compares silicon levels with tissue histologic findings and patient morbidity. One hundred sixty tissue samples were obtained for silicon analysis from 72 patients during augmentation, capsulectomy with or without replacement mammoplasty, mastectomy, or biopsy procedures and were frozen in acid-washed polystyrene tubes at 220 degrees C until analysis. Samples were thawed, sectioned to approximately 0.1 g (dry weight), and digested in nitric acid before analysis by inductively coupled plasma emission spectroscopy, monitoring emission intensity at 251.6 nm. Tissue silicon levels (breast parenchymal and periprosthetic capsular tissue) in patients with silicone gel implants were much higher (mean, 9,287 micrograms/g, n = 106) than in patients with saline implants (mean, 196 micrograms/g, n = 37) or nonaugmented breasts (mean, 64 micrograms/g, n = 17). Histologic examination was performed on 54 tissue samples stained with hematoxylin-eosin. Tissue samples were rated as to degree of inflammation and calcification, and amount of giant cells, foamy histiocytes, and vacuoles containing a colorless refractory material. Vacuolization and foamy histiocyte ratings correlated significantly with tissue silicon concentration. No correlations were found between tissue silicon concentration and inflammation, calcification, or giant cell rating. Implant age (number of years an implant was in place before sampling) correlated with capsular tissue silicon concentration in patients with intact implants but not in those with ruptured implants. No difference in tissue silicon concentration was found between patients with or without signs or symptoms of morbidity. Using 0.1 g of tissue, the method was linear to 1,000 micrograms/g, and sensitivity was 3.7 micrograms/g. Precision between runs (mean, 5.1 micrograms/g; coefficient of variance, 13.7%; n = 13) was calculated from multiple analyses of a bovine liver standard (National Bureau of Standards, reference material 1577a). Significant biologic variability (21.4% to 52.5%) was seen in tissues with high silicon levels. Paraffin-embedded, formalin-fixed tissues are not amenable to silicon analysis by this method, because of leaching of silicone from the tissues during preparation. Thus only fresh frozen tissue samples were used.

Age Factors↗
PubMed2005

Osteoblasts generate harder, stiffer, and more delamination-resistant mineralized tissue on titanium than on polystyrene, associated with distinct tissue micro- and ultrastructure.

UNLABELLED: This study revealed that osteoblasts generate harder, stiffer, and more delamination-resistant mineralized tissue on titanium than on the tissue culture polystyrene, associated with modulated gene expression, uniform mineralization, well-crystallized interfacial calcium-phosphate layer, and intensive collagen deposition. Knowledge of this titanium-induced alteration of osteogenic potential leading to enhanced intrinsic biomechanical properties of mineralized tissue provides novel opportunities and implications for understanding and improving bone-titanium integration and engineering physiomechanically tolerant bone. INTRODUCTION: Bone-titanium integration is a biological phenomenon characterized by continuous generation and preservation of peri-implant bone and serves as endosseous anchors against endogenous and exogenous loading, of which mechanisms are poorly understood. This study determines the intrinsic biomechanical properties and interfacial strength of cultured mineralized tissue on titanium and characterizes the tissue structure as possible contributing factors in biomechanical modulation. MATERIALS AND METHODS: Rat bone marrow-derived osteoblastic cells were cultured either on a tissue culture-grade polystyrene dish or titanium-coated polystyrene dish having comparable surface topography. Nano-indentation and nano-scratch tests were undertaken on mineralized tissues cultured for 28 days to evaluate its hardness, elastic modulus, and critical load (force required to delaminate tissue). Gene expression was analyzed using RT-PCR. The tissue structural properties were examined by scanning electron microscopy (SEM), collagen colorimetry and localization with Sirius red stain, mineral quantification, and localization with von Kossa stain and transmission electron microscopy (TEM). RESULTS: Hardness and elastic modulus of mineralized tissue on titanium were three and two times greater, respectively, than those on the polystyrene. Three times greater force was required to delaminate the tissue on titanium than that on the polystyrene. SEM of the polystyrene culture displayed a porous structure consisting of fibrous and globular components, whereas the titanium tissue culture appeared to be uniformly solid. Cell proliferation was remarkably reduced on titanium. Microscopic observations revealed that the mineralized tissue on titanium was composed of uniform collagen-supported mineralization from the titanium interface to the outer surface, with intensive collagen deposition at tissue-titanium interface. In contrast, tissue on the polystyrene was characterized by collagen-deficient mineralization at the polystyrene interface and calcium-free collagenous matrix formation in the outer tissue area. Such characteristic microstructure of titanium-associated tissue was corresponded with upregulated gene expression of collagen I and III, osteopontin, and osteocalcin mRNA. Cross-sectional TEM revealed the apposition of a high-contrast and well-crystallized calcium phosphate layer at the titanium interface but not at the polystyrene interface. CONCLUSIONS: Culturing osteoblasts on titanium, compared with polystyrene, enhances the hardness, elastic modulus, and interfacial strength of mineralized tissue to a higher degree. Titanium per se possesses an ability to alter cellular phenotypes and tissue micro- and ultrastructure that result in enhanced intrinsic biomechanical properties of mineralized tissue.

Animals↗
PubMed2001

Comparison of the tissue affinity of glucocorticoids to human lung, nasal and skin tissue in vitro.

High affinity binding of topically applied glucocorticoids to their target tissues is the basis for prolonged action of the drug and reduces efflux into the systemic circulation that might account for adverse effects. Since little information on the accumulation and depletion of glucocorticoids to tissues of therapeutic interest is available the binding behavior of different glucocorticoids to human lung, nasal and skin tissue is now evaluated and drug concentrations in different tissues are compared. Furthermore, the role of tissue lipids and proteins in glucocorticoid binding is investigated. Therefore, sliced human lung, nasal and skin tissues are incubated with glucocorticoid containing buffers and time course of adsorption and desorption is monitored. Two model glucocorticoids, the highly lipophilic fluticasone propionate (CAS 80474-14-2) and the rather hydrophilic hydrocortisone (CAS 50-23-7) are compared respecting their binding to native and lipid-depleted tissues. While total adsorption rates to different tissues were highly comparable for each glucocorticoid the observed initial desorption was clearly different. Highest initial depletion was seen for lung tissue, lowest for skin tissue. After initial depletion a prolonged desorption of very low concentrations is observed for all tissues. Lipid depletion of tissues did neither change accumulation not depletion behavior except that about twice as high concentrations were bound and depleted, probably due to protein denaturation. It is concluded that glucocorticoids primarily bind to protein components of human lung, nasal and skin tissues. Connective tissue proteins are discussed to bind glucocorticoids with higher affinity than other protein components, thus preventing high initial release rates. While total amounts of adsorption to different tissues are equivalent and initial desorption of glucocorticoids from saturated tissues varies, highest total remaining concentrations should be observed in skin tissue followed by nasal and lung tissue. Although tissue lipids seem to play no role in total glucocorticoid binding they are suggested to influence the rate constant of uptake and depletion.

Adsorption↗
PubMed1998

Silicon analysis of breast and capsular tissue from patients with saline or silicone gel breast implants: II. Correlation with connective-tissue disease.

The silicone breast implant controversy rages on. Recent work has demonstrated that normal or baseline breast tissue silicon levels in women who had had no prior exposure to any type of breast implant may be as high as 446 microg/gm of tissue. These data ranged from 4 to 446 microg/gm of tissue, with a median of 27.0 microg/gm of tissue. In addition, numerous other epidemiologic and rheumatologic studies have demonstrated no association between silicone breast implants and any connective-tissue diseases. Despite these reports, the use of silicone implants remains restricted. The present study measured breast and capsular tissue silicon levels from 23 breasts in 14 patients with saline implants, and from 42 breasts in 29 patients with silicone implants. No patient in the saline implant group presented with signs or symptoms of connective-tissue disease. Patients with silicone implants, however, were divided into three groups based on the presence or absence of signs or symptoms of connective-tissue disease: group I, no symptoms or signs; group II, + symptoms, no signs; and group III, + symptoms, + signs. Six patients in group III were diagnosed with a specific connective-tissue disease, including systemic lupus erythematosus, rheumatoid arthritis, or scleroderma. The most common indications for implant removal or exchange were capsular contracture and implant rupture, although 41 percent of patients with silicone implants expressed media-related concern over the implant issue. The most common symptoms described by patients in groups II and III were joint pain and stiffness, arm pain and numbness, and fatigue. In all groups, capsular tissue silicon levels were significantly greater than breast tissue levels. This finding may indicate that the capsule serves as a barrier to the distribution of silicone from the implant into adjacent breast tissue. Although breast tissue silicon levels in patients with silicone implants were not significantly greater than those in patients with saline implants (p = 0.48), capsular tissue levels in patients with silicone implants were, indeed, significantly greater than those in patients with saline implants (p < 0.001). However, no statistically significant differences in tissue silicon levels were observed with relation to the presence or absence of connective-tissue disease signs or symptoms in patients with silicone implants (groups I to III). Therefore, these data strengthen the conclusion that there is no association between tissue silicon levels and connective-tissue disease.

Breast↗
PubMed2006

[Analysis on differences between soft-tissue and hard-tissue profile in malocclusions].

OBJECTIVE: To study the characteristics of soft-tissue integument and the differences between soft-tissue and hard-tissue topography in malocclusions. METHODS: 144 female patients, 12-15 years old, were selected. They were divided into class I, class II and class III groups according to the value of angle ANB which was measured on the pre-treatment cephalographs. Each group had 48 patients. Each patient had same type of skeletal pattern and occlusal pattern, full set of permanent teeth and none of cranofacial soft-tissue and hard-tissue diseases. 4 pairs of measurements describing soft-tissue and hard-tissue sagittal facial pattern and the prominence of lips and incisors were measured on each cephalograph. They were angle SnNsB', angle ANB, angle NsSnPos, angleNAPo, UL-SnPos, UI-APo, LL-SnPos and LI-APo. The distribution of soft-tissue sagittal facial pattern in each skeletal group was analyzed. The differences between angle SnNsB' and angle ANB, angle NsSnPos and angle NAPo, UL-SnPos and UI-APo, LL-SnPos and LI-APo were calculated in each patient. Then we calculated the means and the ranges of these differences in each group, the probability of positive and negative difference between each pair of measurements in each group were calculated too. Chi2 test on those probabilities were performed between the three groups. The mean difference between each pair of measurements was then analyzed by ANOVA between the three groups. RESULTS: The disharmony between soft-tissue and hard-tissue sagittal facial pattern was found in 20%-30% of malocclusion patients. There were more or less differences between soft-tissue and hard-tissue topography and the ranges of their variation were quite wide. The soft-tissue integument increasingly tended to augment the convexity of soft-tissue facial profile when skeletal pattern varied from class II to class I to class III, at the same time, tended to increase upper lip prominence and decrease lower lip prominence. CONCLUSION: On the average, soft-tissue integument tends to camouflage the abnormality of hard-tissue topography. But as to individual, the relative independence of soft-tissue integument makes it important to notice the influence of soft tissue on treatment planning and results.

Cephalometry↗