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PubMed1990

Lipoprotein physiology and its relationship to atherogenesis.

The major plasma lipids, cholesterol, triglycerides, and phospholipids are transported as components of macromolecular complexes called lipoproteins. The major lipoprotein classes include the chylomicrons, which transport dietary lipids to the peripheral tissues and the liver; very low density and low density lipoproteins, which transport endogenously synthesized lipids from the liver to peripheral tissues; and high density lipoproteins, which appear to facilitate the reverse transport of cholesterol from peripheral tissues to the liver. The rates of synthesis and catabolism of the major lipoprotein classes are regulated, to a large degree, by one or more proteins, called apoproteins, that reside on the surface of the lipoproteins. This article describes normal lipoprotein metabolism and includes discussions of the role of abnormalities in lipoprotein transport in the atherogenic process.

Animals↗
PubMed2006

[Perioperative thermal management].

Perioperative hypothermia can influence clinical outcome negatively. It triples the incidence of adverse myocardial outcomes, significantly increases perioperative blood loss, significantly augments allogenic transfusion requirements, and increases the incidence of surgical wound infections. The major causes are redistribution of heat from the core of the body to the peripheral tissues and a negative heat balance. Adequate thermal management includes preoperative and intraoperative measures. Preoperative measures, e.g., prewarming, enhance heat content of the peripheral tissues, thereby reducing redistribution of heat from the core to the peripheral tissues after induction of anesthesia. Intraoperative measures are active skin surface warming of a large body surface area with conductive or convective warming systems. Intravenous fluids should be warmed when large volumes of more than 500-1000 ml/h are required. The body surfaces that cannot be actively warmed should be insulated. Airway humidification and conductive warming of the back are less efficient.

Anesthesia↗
PubMed1982

Antibodies to peripheral nerve tissue in sera from patients with acute Guillain-Barré syndrome demonstrated by a mixed haemagglutination technique.

The mixed haemagglutination technique (MA) was used to demonstrate antibodies to peripheral nerve tissue (PNS) in sera from patients with acute Guillain-Barré syndrome (GBS). Within the first 2 weeks of the disease IgG antibodies were detected in sera from 15 of 42 patients (36%). Antibodies were detected in 60% of the patients with severe GBS, and in 30% of those with a mild GBS. The highest titres were found in the sera from the most severely affected patients and could be detected after 48 days of the illness in one of the sera. Sera from healthy blood donors and from patients with various other diseases did not contain antibodies to PNS. The MA technique is reproducible and is more sensitive than the indirect immunofluorescence test and the antiglobulin consumption test.

Antibodies↗
PubMed1995

Localization and identification of granzymes A and B-expressing cells in normal human lymphoid tissue and peripheral blood.

Cytoplasmic granules from activated natural killer (NK) and cytotoxic T lymphocytes (CTL) contain a pore-forming protein, perforin, and several homologous serine proteinases called granzymes. Expression of these proteins correlates with the cytolytic potential of cytotoxic lymphocytes. Using a panel of MoAbs specific for human granzyme A and B, respectively, expression of these proteinases in non-pathological lymphoid tissue and peripheral blood lymphocyte (PBL) subpopulations was investigated. Using immunohistochemistry and double stainings, the phenotype of granzyme-expressing cells in lymphoid tissue was investigated. Granzyme-positive cells were detected in all lymphoid tissues tested. No large differences in the number and distribution between granzyme A- and granzyme B-positive cells were observed. The highest number of positive cells was located in the red pulp of the spleen. Significant numbers were detected in tonsil, lymph nodes, liver and thymus. Low numbers were present in the lamina propria of non-inflamed stomach, small intestine and colon. Phenotypic analysis and cell sorting showed that most of the granzyme-positive cells in lymphoid tissue and PBL consisted of CD3-CD16+CD56+ lymphocytes. Hardly any granzyme-positive CD3+CD8+ CTL were present in peripheral blood. The synthesis of granzyme A as well as B by both CD3+CD16+CD56+ and CD3+CD8+ cells in peripheral blood was increased upon IL-2 stimulation. These results indicate that in normal lymphoid tissue the predominant cytolytic cell population is formed by the NK cells, and activated CTL are rare.

Antibodies, Monoclonal↗
PubMed1996

A suppressive protein generated in peripheral lymph tissue induced by restraint stress.

The results discussed here indicate that under the conditions of restraint stress and under the control of CNS, a suppressive protein (NIP) was generated in peripheral lymph tissue and released into the blood stream, which acts as a immune suppressor. It is potentially a very important molecule that could be very important to our understanding of the interaction between CNS and immune function.

Animals↗
PubMed2006

Chronic administration of belimumab, a BLyS antagonist, decreases tissue and peripheral blood B-lymphocyte populations in cynomolgus monkeys: pharmacokinetic, pharmacodynamic, and toxicologic effects.

The tolerability, pharmacodynamic effects, and pharmacokinetics of belimumab (LymphoStat-B) were evaluated in cynomolgus monkeys. Belimumab is a fully human IgG1lambda antibody directed against B-lymphocyte stimulator (BLyS) protein. BLyS is a TNF family member that supports B-lymphocyte maturation and survival and has been implicated in the pathogenesis of autoimmune diseases and B-lymphocyte malignancies. Belimumab was developed to antagonize BLyS activity in autoimmune diseases and B-lymphocyte malignancies, where undesirable effects of B-lymphocyte activity may cause or contribute to disease. Pharmacodynamic effects of belimumab were monitored by immunophenotyping of peripheral blood. Pathology end points, including tissue immunophenotyping, are described after 13 and 26 weeks of treatment and after a 34-week treatment-free (recovery) period. Belimumab was safe and well tolerated in repeat-dose toxicology studies at 5-50 mg/kg for up to 26 weeks. Monkeys exposed to belimumab had significant decreases in peripheral blood B lymphocytes by 13 weeks of exposure, continuing into the recovery period, despite total lymphocyte counts similar to the controls. There were concomitant decreases in spleen and lymph node B-lymphocyte representation after 13 or 26 weeks of treatment with belimumab. Microscopically, monkeys treated with belimumab for 13 or 26 weeks had decreases in the number and size of lymphoid follicles in the white pulp of the spleen. All findings were generally reversible within a 34-week recovery period. These data confirm the specific pharmacologic activity of belimumab in reducing B lymphocytes in the cynomolgus monkey. The favorable safety profile and lack of treatment-related infections also support continued clinical development of belimumab.

Animals↗
PubMed1976

3H-delta9-tetrahydrocannabinol tissue and subcellular distribution in the central nervous system and tissue distribution in peripheral organs of tolerant and nontolerant dogs.

Tolerant and nontolerant dogs received one i.v. administration of 0.5 mg/kg of 3H-delta9-tetrahydrocannabinol 30 minutes before they were sacrificed. Plasma, peripheral and brain tissues, as well as subcellular fractions of brain tissues from both treatment groups, were analyzed for radioactivity. Throughout the time period before sacrifice, the plasma concentrations of radioactivity in the tolerant and nontolerant dogs were not significantly different. The percentage of radioactivity in brain and plasma that was due to either unchanged delta9-tetrahydrocannabinol or a major metabolite was the same in each group. Of the radioactivity in brain, 46% was identified as delta9-tetrahydrocannabinol. Regardless of treatment, there was a specific accumulation of radioactivity in adrenals, liver, kidney, heart and pancreas. The only significant differences in radioactivity between tolerant and nontolerant peripheral tissues were found in liver, kidney cortex, heart and lymph nodes. Although all brain areas from tolerant dogs contained less radioactivity than the comparable brain areas from nontolerant animals, only pituitary and putamen were significantly less. There was a specific accumulation of radioactivity in some brain areas that could be associated with behavioral effects. The concentration in cerebellar and cerebral gray was significantly greater than that in white, and there was a marked reduction in the concentration in gray after tolerance developed. The mean percentage of radioactivity in each subcellular fraction was as follows: 23% crude nuclei, 44% mitochondria, 8% cholinergic nerve endings, 7% noncholinergic nerve endings, 2% free mitochondria and 6% synaptic vesicles. The quantity of radioactivity in homogenates of brains from tolerant dogs was 17% less than brains of nontolerant animals, which was merely a reflection of the respective plasma concentrations. The distribution of radioactivity was similar in both groups, although most of the subcellular fractions from tolerant dogs contained a lesser amount of radioactivity. The most notable difference was observed in the synaptic vesicle fraction. The synaptic vesicle fraction of tolerant dogs contained 40% less radioactivity than did the same fraction from nontolerant dogs, which implied a possible mechanism of action. A comparison of the remaining subcellular fractions did not appear to explain the development of tolerance.

Animals↗
PubMed1996

Insulin resistance seen in non-insulin dependent diabetes mellitus and hypertension.

The characteristics of NIDDM seen in Japanese is coexistence of diminished insulin secretion and the impaired sensitivity to insulin in the target tissues. Thus, insulin resistance does not mean hyperinsulinemia. To investigate the organ-specific insulin action on glucose homeostasis, we developed an innovative non-invasive method, using an euglycemic hyperinsulinemic clamp combined with oral glucose load. With this procedure, we could reveal muscle glucose uptake and hepatic glucose uptake following oral glucose load, quantitatively, separately and simultaneously. The effect of strict glycemic control in non-obese NIDDM who were secondary failure to sulfonylurea with 3 times prandial regular insulin injections, on glucose disposals are investigated. Glucose disposal by peripheral tissues was not altered (clamped blood glucose and insulin concentration are, 90 mg/dl and 200 microU/ml, respectively). The ratio of splanchnic glucose disposal to the amount of ingested glucose, on the other hand, significantly increased to 33.1% from 14.5%. Therefore, short-term strict glycemic control appears to improve glucose handling by splanchnic tissues without affecting insulin sensitivity of peripheral tissues in NIDDM. This method would be feasible to investigate whether insulin resistance seen in hypertensive patients, is located only in peripheral tissues or is also in the liver. To find patients with asymptomatic atherosclerosis, we routinely apply a noninvasive maneuver using high resolution B-mode imaging of the carotid artery, to determine atherosclerosis quantitatively. Impaired glucose tolerance (IGT) male subjects showed significantly greater thickness of the intimal plus medial complex (IMT) than age-matched healthy males and showed no significant differences compared to age-matched NIDDM patients. Among IGT, those with exaggerated insulin secretion (average serum insulin concentration was 100 microU/ml at 1 and 2 h after), in other words, insulin resistant, showed thicker IMT. The characteristics of IGT groups with high insulin level were, BMI more than 25, diastolic blood pressure more than 83 mmHg, serum triglyceride more than 215 mg/dl. Thus, among mildly obese, mild hypertensive, mild glucose intolerant, slightly hypertriglyceridemic Japanese male subjects, there exist advanced atherosclerotic subjects.

Arteriosclerosis↗
PubMed1998

Lung cancer patients have increased 8-hydroxydeoxyguanosine levels in peripheral lung tissue DNA.

The 8-hydroxydeoxyguanosine (8-OH-dG) levels in the peripheral parts of human lung tissues were compared between lung cancer patients (n=70) and non-cancer patient controls (n=15). An increased level of 8-OH-dG was observed in the lung cancer group, in both the adenocarcinoma and non-adenocarcinoma (mainly squamous cell carcinoma) groups, as compared to the non-cancer control group. This result suggests that reactive oxygen species are partly involved in the induction of lung carcinomas (both adenocarcinoma and non-adenocarcinoma).

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1992

Pharmacokinetics of fluorinated 2-nitroimidazole hypoxic cell radiosensitizers in murine peripheral nervous tissue.

We have previously reported that KU-2285, a 2-nitroimidazole with a fluorinated N1-substituent (-CH2-CF2CONH(CH2)nOH, n = 2), was a promising hypoxic cell radiosensitizer. In this study the pharmacokinetics of KU-2285 and its related compounds (n = 3 and n = 4) were compared with those of etanidazole (a 2-nitroimidazole with an N1-substituent of -CH2CONH(CH2)nOH, n = 2) and its related compounds (n = 3 and n = 4) to assess the effects of incorporation of a CF2 group. The lipophilicity of the fluorinated compounds was higher than that of etanidazole, as measured by the octanol/water partition coefficient. As the number of CH2 groups increased, the lipophilicity of the compounds in both the KU-2285 and etanidazole series increased. The brain tissue levels of the fluorinated compounds were as low as those of the etanidazole derivatives, while the biological half-lives of the fluorinated compounds in peripheral nervous tissues were shorter than those of related non-fluorinated compounds.

Animals↗
PubMed1981

A comparison of demyelinating and myelination-inhibiting factor induction by whole peripheral nerve tissue and P2 protein.

Sera from rabbits sensitized with whole bovine spinal roots demyelinated and inhibited myelination in both peripheral and central nervous system tissue cultures. Antisera directed against the peripheral nerve myelin basic protein, P2, demonstrated no antimyelin activity in vitro. These results suggest that demyelinating and myelination-inhibiting factors are directed against some peripheral nerve component(s) other than the P2 protein.

Animals↗
PubMedDate not supplied

Evidence for neurotensin as a non-adrenergic, non-cholinergic neurotransmitter in guinea pig ileum.

Neurotensin is a 13-amino acid peptide that is widely distributed in central and peripheral tissues of various mammalian species. In peripheral tissues, the highest concentration of neurotensin-like immunoreactivity is found in the ileum, where it is present in endocrine-like cells and nerve fibres. The longitudinal smooth muscle layer of the guinea pig ileum, where neurotensin has both a direct relaxant and an indirect contractile action, has been used extensively as a biological assay system for neurotensin. We report here that the majority of specific 3H-neurotensin binding sites is present in the guinea pig ileum circular smooth muscle layer, which is known to be innervated by a large proportion of the ileal non-adrenergic inhibitory nerves. Neurotensin produces a dose-dependent, tetrodotoxin-resistant relaxation, whereas the relaxation produced by field stimulation of the inhibitory nerves is frequency-dependent and tetrodotoxin-sensitive. The calcium-dependent potassium channel blocker apamin inhibits both the neurotensin- and nerve stimulation-induced muscle relaxation. Incubation of the circular smooth muscle preparation with a neurotensin antiserum substantially inhibited the nerve stimulation-induced relaxation, indicating a direct relationship between the effects of neurotensin and of nerve stimulation.

Animals↗
PubMed1986

Plasma branched-chain keto acids in burn patients.

Plasma branched-chain keto acids (BCKA) and glucose-alanine cycle-related substances were measured in venous and arterial blood following burn injury. It was found that the three BCKA diminished with a minimum on day 7 while pyruvate increased. Alanine and glutamate + glutamine also decreased but plasma branched-chain amino acids (BCAA) did not vary. BCKA and gluconeogenic amino acids were liberated by peripheral tissues whereas BCAA were not. By analogy with the fate of alanine, a reduction in plasma BCKA associated with a high release by peripheral tissues might involve an increase in their hepatic metabolism. The BCKA would then give rise to ketone bodies used by the peripheral tissue. This step would complete the glucose-alanine cycle described by Cahill in hypercatabolic states where energy requirements are intense and similar to those found in burn injuries.

Adolescent↗
PubMed1986

Tissue differences in the up-regulation of glucocorticoid-binding proteins in the rat.

The magnitude of increase in glucocorticoid receptor concentration and transcortin-like binding was examined in a variety of peripheral tissues and brain structures after adrenalectomy. Glucocorticoid binding was assayed in liver, heart, kidney, pituitary, hippocampus, cerebral cortex, amygdala-entorhinal area, and hypothalamus. Glucocorticoid receptor concentration, measured using [3H]dexamethasone as ligand, increased in all eight tissues, but the magnitude of this increase varied 30-fold among tissues. The largest increase was shown by kidney cytosol, followed by amygdala-entorhinal cortex, hippocampus, liver, cerebral cortex, hypothalamus, pituitary, and heart. These increases were not due to a selective enhancement of mineralocorticoid receptors. The increase in transcortin in peripheral tissues was variable and exceeded the increase in plasma transcortin by an order of magnitude. It was concluded that up-regulation of the glucocorticoid receptor after adrenalectomy is a response common to most, if not all, glucocorticoid target tissues. However, the magnitude of this response was tissue specific and was not directly related to initial receptor density. The marked increase in tissue transcortin ([3H]corticosterone binding in the presence of excess dexamethasone) suggested that plasma transcortin is sequestered by peripheral tissues in substantial amounts in the acutely adrenalectomized rat. The increase in transcortin uptake by tissues and the increases in cytosolic receptor number are apparently subject to different regulatory control.

Adrenalectomy↗
PubMed1992

Differential tissue regulation of the insulin-like growth factors in rats bearing the MStT/W15 pituitary tumor.

The content of insulin-like growth factors, IGF-I and IGF-II, was measured in tissues of rats bearing a transplantable mammosomatotrophic tumor, MStT/W15. Serum IGF-I was elevated in tumor-implanted rats [2,557 +/- (SE) 419 vs. 891 +/- 100 ng/ml], and tumor tissue concentrations of IGF-I were increased (321 +/- 16 ng/g) in comparison to control liver tissue (160 +/- 5 ng/g) or control pituitary (80 +/- 3 ng/g). The IGF-I levels were significantly increased in most peripheral tissues in the tumor-bearing rats with the exception of the liver. In support of this finding, messenger RNA for prepro IGF-I was likewise not increased in the livers of tumor-bearing rats, nor was there an increase in the growth hormone-dependent IGF-binding protein, BP-3, in the liver or serum of these animals. All tumors had detectable levels of prepro IGF-I mRNA which was, however, less than 50% of that noted in normal control liver. The tumors also expressed an IGF-BP which was identified as IGF-BP-2 by immunoblotting. Serum concentrations of IGF-II were similar in control and tumor-bearing animals (approximately 70 ng/ml). IGF-II levels in the tumor (90 +/- 5 ng/g) were significantly higher than levels in control liver (34 +/- 2 ng/g), but similar to those found in normal pituitary (165 +/- 24 ng/g). In peripheral tissues, IGF-II concentrations were selectively increased in skeletal muscle and heart of tumor-bearing rats. These data demonstrate tissue-specific regulation of IGF-I and IGF-II. Paradoxically, the liver does not appear to be stimulated over control levels by high serum growth hormone levels, since neither IGF-I peptide, IGF-I mRNA, nor IGF-BP-3 levels are increased in livers of tumor-bearing rats. This suggests that the increase in serum IGF-I in these animals is due to increased production of IGF-I by the tumors themselves and by nonhepatic peripheral tissues and further that hepatic responsiveness to growth hormone is diminished in these tumor-bearing animals.

Animals↗
PubMed2006

Molecular components of the mammalian circadian clock.

Circadian rhythms are approximately 24-h oscillations in behavior and physiology, which are internally generated and function to anticipate the environmental changes associated with the solar day. A conserved transcriptional-translational autoregulatory loop generates molecular oscillations of 'clock genes' at the cellular level. In mammals, the circadian system is organized in a hierarchical manner, in which a master pacemaker in the suprachiasmatic nucleus (SCN) regulates downstream oscillators in peripheral tissues. Recent findings have revealed that the clock is cell-autonomous and self-sustained not only in a central pacemaker, the SCN, but also in peripheral tissues and in dissociated cultured cells. It is becoming evident that specific contribution of each clock component and interactions among the components vary in a tissue-specific manner. Here, we review the general mechanisms of the circadian clockwork, describe recent findings that elucidate tissue-specific expression patterns of the clock genes and address the importance of circadian regulation in peripheral tissues for an organism's overall well-being.

Animals↗
PubMed1985

Effects of insulin on peripheral and splanchnic glucose metabolism in noninsulin-dependent (type II) diabetes mellitus.

The mechanism(s) and site(s) of the insulin resistance were examined in nine normal-weight noninsulin-dependent diabetic (NIDD) subjects. The euglycemic insulin clamp technique (insulin concentration approximately 100 microU/ml) was employed in combination with hepatic and femoral venous catheterization and measurement of endogenous glucose production using infusion of tritiated glucose. Total body glucose metabolism in the NIDD subjects (4.37 +/- 0.45 mg/kg per min) was 38% (P less than 0.01) lower than in controls (7.04 +/- 0.63 mg/kg per min). Quantitatively, the most important site of the insulin resistance was found to be in peripheral tissues. Leg glucose uptake in the diabetic group was reduced by 45% as compared with that in controls (6.0 +/- 0.2 vs. 11.0 +/- 0.1 mg/kg leg wt per min; P less than 0.01). A strong positive correlation was observed between leg and total body glucose uptake (r = 0.70, P less than 0.001). Assuming that muscle is the primary leg tissue responsible for glucose uptake, it could be estimated that 90 and 87% of the infused glucose was disposed of by peripheral tissues in the control and NIDD subjects, respectively. Net splanchnic glucose balance during insulin stimulation was slightly more positive in the control than in the diabetic subjects (0.31 +/- 0.10 vs. 0.05 +/- 0.19 mg/kg per min; P less than 0.07). The difference (0.26 mg/kg per min) in net splanchnic glucose balance in NIDD represented only 10% of the reduction (2.67 mg/kg per min) in total body glucose uptake in the NIDD group and thus contributed very little to the insulin resistance. The results emphasize the importance of the peripheral tissues in the disposal of infused glucose and indicate that muscle is the most important site of the insulin resistance in NIDD.

Biological Transport↗