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PubMed1996

[MR tomography (MRT) of the skeleton, peripheral soft tissues and joints--current overview].

A review: The skeleton, the peripheral soft tissues, and the joints have become important indications to use MRI routinely. About 25-35% of daily examinations focus on these anatomic sites. Superior contrast resolution, the option of different imaging planes, and the unsurpassed visualization of bone marrow, fibrous and hyaline cartilage, ligaments, and tendons are the reasons for the overwhelming success of this imaging method. MRI often provides the direct way to diagnosis. More and more the so-called "step by step" approach to diagnosis by imaging methods is being abandoned in favor of the primary use of MRI. The present survey summarizes the main indications for MRI in the field of the musculoskeletal system, in adults as well as in children. Special topics like tumors, inflammation, ischemia, and trauma are discussed. Some anatomic sites like the carpal joint, the shoulder, and the knee are presented in more detail.

Adult↗
PubMed1977

Correlation between inhibition of indicator cell migration and tuberculin hypersensitivity in patients with suspected tuberculous inflammation of the uveal tissue.

Peripheral blood lymphocytes from patients with suspected tuberculous inflammation of the uveal tissue were examined for their capacity to produce in vitro a migration inhibition factor in the presence of specific antigen. Three modifications of the capillary tube migration technique were used to demonstrate MIF. The indicator cells were guinea pig peritoneal macrophages and human peripheral blood leucoytes. A correlation was found between the migration of indicator cells influenced by lymphocytes from Mantoux-positive donors in the presence of specific antigen and the tuberculin sensitivity. The possible uses of the in vitro tests as a correlate to cellular hypersensitivity in vivo in the human system are discussed.

Animals↗
PubMed1984

Relationship between levels of nerve growth factor (NGF) and its messenger RNA in sympathetic ganglia and peripheral target tissues.

We have developed a sensitive assay for the quantification of nerve growth factor mRNA (mRNANGF) in various tissues of the mouse using in vitro transcribed RNANGF. Probes of both polarities were used to determine the specificity of the hybridization signals obtained. Comparison of NGF levels with its mRNA revealed that both were correlated with the density of sympathetic innervation. Thus, vas deferens contained high levels of both NGF and mRNANGF, whereas skeletal muscle levels were barely detectable, indicating that in peripheral tissues NGF levels are primarily regulated by the quantity of mRNANGF and not by the rate of processing of NGF precursor to NGF. However, although superior cervical ganglia contained the highest levels of NGF, its mRNA was barely detectable. Thus, the high levels of NGF in sympathetic ganglia result from retrograde axonal transport rather than local synthesis. The quantity of NGF found in the submandibular glands of female animals was three orders of magnitude higher than expected from their mRNA levels. This observation is discussed in the context of the difference between the mechanism of storage and exocytosis of exocrine glands versus the constitutive release from other tissues.

Animals↗
PubMed1988

Tissue specific regulation of "peripheral-type" benzodiazepine receptor density after chemical sympathectomy.

The characteristics of [3H]Ro 5-4864 binding to "peripheral" benzodiazepine receptors (PBR) in the central nervous system and peripheral tissues were examined after chemical sympathectomy with 6-hydroxydopamine (6-OHDA). One week after the intracisternal administration of 6-OHDA, the number of [3H]Ro 5-4864 binding sites (Bmax) in the hypothalamus and striatum increased 41 and 50%, respectively, concurrent with significant reductions in catecholamine content. An increase (34%) in the Bmax of [3H]Ro 5-4864 to cardiac ventricle was observed one week after parenteral 6-OHDA administration. In contrast, the Bmax of [3H]Ro 5-4864 to pineal gland decreased 48% after 6-OHDA induced reduction in norepinephrine content. The Bmax values for [3H]Ro 5-4864 binding to other tissues (including lung, kidney, spleen, cerebral cortex, cerebellum, hippocampus and olfactory bulbs) were unaffected by 6-OHDA administration. The density of pineal, but not cardiac PBR was also reduced after reserpine treatment, an effect reversed by isoproterenol administration. These findings demonstrate that alterations in sympathetic input may regulate the density of PBR in both the central nervous system and periphery in a tissue specific fashion.

Animals↗
PubMed1990

Flow cytometric and immunohistochemical characterization of the gamma/delta T-lymphocyte population in normal human lymphoid tissue and peripheral blood.

We determined the quantitative and topographic distribution of gamma/delta lymphocytes in normal human lymphoid tissue and peripheral blood using a monoclonal antibody that detects a framework determinant on delta molecules and delineated the immunophenotypic characteristics of the gamma/delta lymphocyte population by one- and/or two-color immunohistochemical and two- and/or three-color flow cytometric analysis. Variable, but generally small, numbers of gamma/delta lymphocytes are present in peripheral blood and in all lymphoid tissues. The vast majority, greater than or equal to 90%, of lymphoid tissue delta lymphocytes reside in interfollicular (T-cell) zones. Approximately 90% of delta thymocytes are present in the thymic medulla. The percentage of CD3-positive T cells that express delta are: spleen 12.5 +/- 8.1%, peripheral blood 4.0 +/- 3.1%, appendix 2.9 +/- 1%, lymph node 2.2 +/- 1%, thymus 1.4 +/- 0.5%, and tonsil 0.7 +/- 0.5%. We further demonstrated that 1) gamma/delta-thymocytes and gamma/delta peripheral lymphocytes express T-cell lineage restricted antigens CD3 and CD2 but only a variable subset, 30% to 90%, express T-cell lineage associated antigens CD5 and/or CD8; (2) approximately 60% of gamma/delta thymocytes express low-density CD4 while all gamma/delta peripheral lymphocytes lack detectable CD4; 3) gamma/delta lymphocytes lack natural killer (NK), macrophage, and B-cell associated antigens CD16, CD14, and CD20, respectively, but greater than or equal to 70% of gamma/delta T lymphocytes express CD11b, Leu7, and NKH-1, antigens, which are also expressed by suppressor/cytotoxic and NK cells; and 4) a large subpopulation, approximately 25%, of gamma/delta thymocytes are in S1-G2 phase, while greater than or equal to 98% of gamma/delta peripheral lymphocytes are small lymphocytes in G0-G1 phase and lack activation/proliferation markers. Together these results indicate that gamma/delta lymphocytes are resting, mature T cells that probably play a primary role in suppressor/cytotoxic phenomena. They also indicate that gamma/delta lymphocytes variably express multiple-cell surface antigens associated with various cell lineages, suggesting that gamma/delta lymphocytes represent a considerably more heterogeneous cell population than previously appreciated and that they may actually subserve multiple functions.

Animals↗
PubMed2001

Influence of chronic inflammation in peripheral target tissue on recovery of crushed nerve injury.

An experimental study was performed to investigate the influence of chronic inflammation in peripheral target tissue on recovery of the sciatic nerve after crush injury. Thirty-four male Wistar rats, weighing 300-370 g were used. The sciatic nerve was crushed unilaterally with an aneurysm clip (250 gf; holding force; 5 min). One week before the operation, chronic inflammation, localized in the tibiotarsal joint of one hind limb, was produced by the intraarticular injection of complete Freund's adjuvant. The animals were divided into five groups, as follows: CIA (crush injury with ipsilateral arthritis), CCA (crush injury with contralateral arthritis), C (crush injury without arthritis), A (sham operation and ipsilateral arthritis), and S (sham operation without arthritis). Specimens for histological examination were taken from the nerve at a site 5 mm distal to the crush injury 4 weeks postoperatively. Histological study showed that the diameters of the axons in group CIA were significantly smaller than those in group CCA and those in group C. No significant differences were observed between group CCA and group C. In conclusion, peripheral nerve recovery after crush injury was suppressed by chronic inflammation in peripheral target tissue.

Animals↗
PubMed2006

[Insulin resistance in non-alcoholic fatty liver disease].

Insulin resistance is the pathophysiological hallmark of various kinds of clinical diseases, including non- alcoholic fatty liver disease. Insulin resistance is the common characteristic of metabolic syndrome and its related features. Insulin resistance is a systemic disease that affects the nervous system, muscles, pancreas, kidney, heart and immune system, in addition to the liver. A complex interaction between genes and environment factors enhances insulin resistance and the phenotypic expression of NAFLD (non- alcoholic fatty liver disease) in individual patients. Advanced fibrotic liver disease is associated with many features of metabolic syndrome, and the risk of progressive liver disease should not be underestimated for the individuals suffering with metabolic disorders. Abnormalities of insulin signaling can cause the state of insulin resistance, but there is no clear cut scientific evidence that distorted insulin signaling is the primary pathophysiological defect. Increased adipose tissue mass can cause peripheral tissue insulin resistance via the changes of the adipocytokine secretory patterns. We discuss in this article the sequences of the insulin signaling cascades and the possible molecular targets of insulin resistance, the humoral "cross talk" between the distorted secretory patterns of the adipocytokines, and the peripheral tissue insulin resistance along with the pathophysiology of NAFLD.

Adipose Tissue↗
PubMed1992

Sepsis-induced insulin resistance in rats is mediated by a beta-adrenergic mechanism.

Bacterial infection decreases insulin-mediated glucose uptake (IMGU) by skeletal muscle and produces whole body insulin resistance. Because circulating catecholamines are elevated by the septic insult, the present study was performed to determine the potential role of the beta-adrenergic system in eliciting these changes. Before induction of sepsis, an infusion containing saline, propranolol, or atenolol was started and continued throughout the experimental protocol. Sepsis increased the basal rate of glucose production and utilization and impaired IMGU by peripheral tissues. The peripheral insulin resistance in septic rats was manifested by an increase in the dose producing 50% of maximal response and a decrease in the maximal responsiveness. Infusion of propranolol, a nonselective beta-adrenergic antagonist, attenuated the sepsis-induced increase in basal glucose turnover by 70% and completely prevented the decrease in IMGU by the whole body. In contrast, atenolol, a selective beta 1-antagonist, did not alter the glucose metabolic response to infection. Under basal conditions, propranolol prevented or attenuated the increase in glucose uptake by the gastrocnemius, diaphragm, skin, liver, lung, spleen, and ileum normally observed in septic rats. In addition, propranolol prevented the decrease in IMGU by various muscles and skin in septic animals. These results suggest that adrenergic stimulation, probably mediated by a beta 2-adrenergic mechanism, is partially responsible for the sepsis-induced increases in basal whole body glucose turnover and plays a prominent role in the development of peripheral insulin resistance in this condition.

Animals↗
PubMed1984

The comparative distribution of xenopsin- and neurotensin-like immunoreactivity in Xenopus laevis and rat tissues.

The regional distribution of xenopsin-like immunoreactivity (XPLI) and of neurotensin-like immunoreactivity (NTLI) was studied by radioimmunoassay in tissues of Xenopus laevis and rat. In Xenopus laevis, XPLI showed a wide distribution throughout central and peripheral tissues with the highest concentration in the skin; NTLI was found in both central and peripheral tissues with the exception of the skin. Gel chromatography on Sephadex G-25 was used in order to characterize the immunoreactive material; both XPLI and NTLI eluted in a single peak at the position of synthetic xenopsin and neurotensin. No XPLI could be detected in central and peripheral tissues from mouse, rat, guinea-pig, rabbit or cat. In contrast, NTLI was found in a variety of peripheral tissues of the rat and it coeluted with synthetic neurotensin on reverse phase high-performance liquid chromatography. It is probably present in preganglionic parasympathetic nerve fibres.

Animals↗
PubMed2006

Differential sensitivity of blood, peripheral, and central cholinesterases in beagle dogs following dietary exposure to chlorpyrifos.

Two studies were performed to find out whether exposure limits that protect brain acetylcholinesterase (AChE) will protect peripheral tissue AChE after exposure to chlorpyrifos (CPF), an organophosphate insecticide. In a methods-development study, male dogs (3/dose) were exposed to 0.0, 0.3, 0.6, or 1.2mg/kg/day CPF in their diets for 4 weeks. Mixed cholinesterase (mChE), AChE, and butyrylcholinesterase (BuChE) activities were measured in plasma, RBC, brain, left atrium and ventricle, diaphragm, quadriceps, and nodose ganglia. Plasma, brain and peripheral tissue BuChE was inhibited at all dose levels. While RBC AChE was inhibited at all doses, brain and peripheral AChE activities were unaffected. In the main study, dogs (4/sex/dose) were exposed to 0.0, 0.5, 1.0, or 2.0mg/kg/day CPF in their diets for six weeks and RBC AChE was significantly inhibited at all doses in both sexes. Diaphragm, quadriceps, and nodose ganglia AChE was unaffected by treatment. Brain AChE was decreased by approximately 6% compared to controls in high-dose groups, and this was considered a threshold effect. Left atrium AChE in high-dose dogs was 25.5% less (males) and 32.1% greater (females) than controls; these differences were attributed to chance. While peripheral tissue and brain AChE were not affected following exposure to 1.0mg/kg/day, RBC AChE was inhibited at all doses. These results show that RBC AChE is more sensitive than brain or peripheral tissue AChE to inhibition by CPF, and that protection of brain AChE would protect peripheral tissue AChE.

Animals↗
PubMed1991

Tissue oxygenation in hemorrhagic shock measured as transcutaneous oxygen tension, subcutaneous oxygen tension, and gastrointestinal intramucosal pH in pigs.

BACKGROUND AND METHODS: Tissue oxygenation, measured in peripheral tissue as transcutaneous PO2 (PtCO2) and subcutaneous PO2, was compared with the oxygenation in GI mucosa, which was measured as intramucosal wall pH (pHi), during experimental hemorrhagic shock and resuscitation in pigs. The pigs were hemorrhaged stepwise to a BP of 80 and 45 mm Hg, followed by retransfusion. PtCO2 was measured in the groin and subcutaneous PO2 was measured in the hip region. Intraluminal PCO2 was measured in the stomach, in the small intestine, and the sigmoid colon using silicone catheters. A simultaneous determination of arterial blood HCO3 concentration allowed pHi to be calculated using Henderson-Hasselbalch equation. Cardiac output was determined by thermodilution, and oxygen delivery (DO2) was calculated. RESULTS: Early indications of shock were decreases in PtCO2 and intestinal pHi (p less than .01). All measured variables decreased at the second step of bleeding. PtCO2 and subcutaneous PO2 was correlated to DO2 through the entire experiment (r2 = .25 and .49, respectively). Also, the pHi of the small intestine and the sigmoid colon correlated with DO2 (r2 = .36 and .25, respectively). PtCO2 and subcutaneous PO2 correlated with pHi in the small intestine and sigmoid colon. CONCLUSIONS: PtCO2 and pHi in the small intestine and sigmoid colon were the variables that most rapidly indicated blood volume loss. Subcutaneous PO2 and PtCO2, and small intestine and sigmoid colon pHi were correlated to total body oxygen transport. Peripheral tissue perfusion followed intestinal perfusion to some extent.

Animals↗
PubMed1985

Distribution of cathepsins B and H in rat tissues and peripheral blood cells.

The concentrations of cathepsins B and H in various tissues and peripheral blood cells of rats were determined by means of sensitive immunoassays. The minimum detectable amounts of cathepsins B and H were 30 pg and 20 pg/assay, respectively, and the presence of endogenous thiol proteinase inhibitors did not interfere with the immunoassays. Cathepsin B was found at high levels in the kidney, vagina, spleen, and adrenal gland, and cathepsin H at high levels in the kidney, vagina, liver, lung, and spleen. Low levels of cathepsins B and H were present in the heart, skeletal muscle, and testis. The ratios of cathepsins B and H in various organs were different: the brain and adrenal gland contained much higher levels of cathepsin B than of cathepsin H, whereas the lung and liver contained higher levels of cathepsin H than of cathepsin B. In several organs such as the kidney, spleen, liver, and lungs, the level of cathepsins B plus H was much higher than that of thiol proteinase inhibitors (TPI-alpha + TPI-beta), whereas in tissues containing large amounts of TPI-alpha, such as the skin, esophagus and stomach, the level of inhibitors was higher than that of cathepsins B plus H. Of the peripheral blood cells tested, macrophages had the highest contents of cathepsins B and H, and so their level of cathepsins B plus H was much higher than that of TPI-alpha plus TPI-beta, whereas lymphocytes and neutrophils contained comparable amounts of proteinases and inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Establishment and maintenance of a longitudinal study of bovine spongiform encephalopathy (the ULiSES scheme).

This paper addresses the issues of tracing and compliance encountered in setting up and maintaining a UK-wide 5-year observational study of beef cattle. The 5-year prospective study was initiated in 1997 to investigate the occurrence of bovine spongiform encephalopathy (BSE) in a single herd of pedigree Aberdeen Angus cattle, in which BSE had been detected at low prevalence. The study was given the acronym ULiSES (University of Liverpool Spongiform Encephalopathy Scheme). All cattle present on the farm at the start of the scheme were registered as members of the study population (n=320), as were all calves subsequently born on the farm (n=350). Animals that were sold (n=291) were traced and monitored at destination farms. Farmers were requested to give advance notification of slaughter of any ULiSES animal and an attempt was made to collect post-mortem samples of nervous tissue, peripheral lymphoid tissue and striated muscle from all animals in the scheme at the time of slaughter, death or euthanasia. Sections of medulla were examined (by standard histopathological techniques) for the presence of spongiform change. Remaining samples were stored at -70 degrees C for future investigation by alternative tests. At the halfway point of the scheme in October 1999, 75.2% (506/673) of the study population was still alive; 42% (284) of the population was still alive on the study farm and 33% (222) was distributed on other farms throughout the UK. Complete sets of specimens had been recovered from 77% (129/167) of dead animals. All brainstem sections were negative by histopathological examination. No suspect cases of BSE were reported in ULiSES animals. Failure to recover specimens occurred principally in animals which had left the study farm. The main cause of specimen loss was a failure of compliance in a small number of individuals who had purchased large numbers of ULiSES animals, and subsequently slaughtered them without contacting the University. Despite this, farmer compliance was generally high. The ULiSES scheme shows the feasibility of a country-wide longitudinal observational study spanning a period of several years and indicates the large impact of small numbers of non-compliant individuals.

Animals↗
PubMed2003

Possible involvement of opioid receptors in moclobemide-induced hypothermia in mice.

Effect of moclobemide, a selective monoamine oxidase-type A enzyme inhibitor, was investigated on the body temperature of male mice. Moclobemide (15-30 mg kg(-1), i.p.) produced significant reductions of body temperature in both normal and yeast-induced hyperthermic male mice. The hypothermic effect of moclobemide was moderate and short-lasting. Moclobemide-induced hypothermia was not antagonized by previous administration of prazosin (10 and 20 mg kg(-1), s.c.), propranolol (5, 10, and 20 mg kg(-1), s.c.), haloperidol (2 and 10 mg kg(-1), s.c.), atropine (10 and 20 mg kg(-1), s.c.), mepyramine (25 and 50 mg kg(-1), s.c.), or methysergide (0.5, 1, and 2 mg kg(-1), s.c.). Pretreatment with the opioid antagonist naloxone (10 mg kg(-1), s.c.), however, was able to reverse the hypothermic effect of moclobemide (30 mg kg(-1), i.p.) in both normal and yeast-induced hyperthermic mice. The present results indicate a possible role for central opioid receptors in the hypothermic effect of moclobemide. Also, a peripheral component for this effect of moclobemide at the mitochondria of peripheral tissues is suspected. The peripheral tissue mitochondria could be considered a common target for moclobemide and opioids actions on body temperature.

Animals↗
PubMed2002

New antidepressant drugs that do not cross the blood-brain barrier.

Stimulation of neurogenesis in the adult brain (i.e. in the hippocampus) has recently been proposed as a putative mechanism of antidepressant action of drugs. This effect of antidepressants may not be achieved by their primary action on proliferating cells, but may involve the drug-triggered mobilization of trophic factors, such as brain-derived neurotrophic factor (BDNF), glia-derived protein S100 beta, or insulin-like growth factor I (IFG-I). Whereas BDNF and S100 beta are produced in the brain, IGF-I is primarily released from peripheral tissues. Administered peripherally, IGF-I increases hippocampal neurogenesis in the adult rat. Because synthesis and release of IGF-I appear to be stimulated by serotonergic mechanisms, we propose that antidepressants that affect serotonergic mechanisms might be rendered more effective by mobilizing IGF-I. Moreover, we suggest that new antidepressant drugs could be designed that would not enter into the brain but would stimulate peripheral mediators such as IGF-I.

Animals↗
PubMed1996

Human ryudocan from endothelium-like cells binds basic fibroblast growth factor, midkine, and tissue factor pathway inhibitor.

Ryudocan, a heparan sulfate proteoglycan, was isolated from human endothelium-like EAhy926 cells by a combination of ion-exchange and immunoaffinity chromatography. Purified human ryudocan has biochemical properties similar to those of rat ryudocan isolated from microvascular endothelial cells. Human ryudocan contains only heparan sulfate (HS) glycosaminoglycan chains along with a core protein with an apparent molecular mass of 30 kDa. We evaluated the interactions between purified human ryudocan and several extracellular ligands by using a solid-phase binding assay. We found that basic fibroblast growth factor (bFGF), midkine (MK), and tissue factor pathway inhibitor (TFPI) exhibit significant ryudocan binding. Heparitinase (but not chondroitin ABC lyase) treatment destroyed the ability of ryudocan binding to bFGF, MK, and TFPI. Heparin and HS, but not chondroitin sulfate, inhibited such ryudocan binding. Thus, the HS chains of ryudocan appear to be responsible for its binding to bFGF, MK, and TFPI. The apparent dissociation constants for purified ryudocan were as follows: bFGF, 0.50 nM; MK, 0.30 nM; and TFPI, 0.74 nM. Immunohistochemical analysis revealed that ryudocan was expressed in fibrous connective tissues, peripheral nerve tissues, and placental trophoblasts. These findings suggest that ryudocan may possess multiple biological functions, such as bFGF modulation, neurite growth promotion, and anticoagulation, via HS-binding effectors in the cellular microenvironment.

Amino Acid Sequence↗
PubMed1992

Quantitative analysis of amino acid oxidation and related gluconeogenesis in humans.

Significant gaps remain in our knowledge of the pathways of amino acid catabolism in humans. Further quantitative data describing amino acid metabolism in the kidney are especially needed as are further details concerning the pathways utilized for certain amino acids in liver. Sufficient data do exist to allow a broad picture of the overall process of amino acid oxidation to be developed along with approximate quantitative assessments of the role played by liver, muscle, kidney, and small intestine. Our analysis indicates that amino acids are the major fuel of liver, i.e., their oxidative conversion to glucose accounts for about one-half of the daily oxygen consumption of the liver, and no other fuel contributes nearly so importantly. The daily supply of amino acids provided in the diet cannot be totally oxidized to CO2 in the liver because such a process would provide far more ATP than the liver could utilize. Instead, most amino acids are oxidatively converted to glucose. This results in an overall ATP production during amino acid oxidation very nearly equal to the ATP required to convert amino acid carbon to glucose. Thus gluconeogenesis occurs without either a need for ATP from other fuels or an excessive ATP production that could limit the maximal rate of the process. The net effect of the oxidation of amino acids to glucose in the liver is to make nearly two-thirds of the total energy available from the oxidation of amino acids accessible to peripheral tissues, without necessitating that peripheral tissues synthesize the complex array of enzymes needed to support direct amino acid oxidation. As a balanced mixture of amino acids is oxidized in the liver, nearly all carbon from glucogenic amino acids flows into the mitochondrial aspartate pool and is actively transported out of the mitochondria via the aspartate-glutamate antiport linked to proton entry. In the cytoplasm the aspartate is converted to fumarate utilizing urea cycle enzymes; the fumarate flows via oxaloacetate to PEP and on to glucose. Thus carbon flow through the urea cycle is normally interlinked with gluconeogenic carbon flow because these metabolic pathways share a common step. Liver mitochondria experience a severe nonvolatile acid load during amino acid oxidation. It is suggested that this acid load is alleviated mainly by the respiratory chain proton pump in a form of uncoupled respiration.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗