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PubMedDate not supplied

Transfer index of MR relaxation enhancer: a quantitative evaluation of MR contrast enhancement.

To clarify the effects of Gd-DTPA on biological water, we examined the effects of the compound on spin-lattice relaxation rate with various concentrations of gelatin solutions. The results indicate that the effects of relaxation rate of Gd-DTPA in biological water fundamentally correspond to those in aqueous solution. To evaluate the distribution of Gd-DTPA in tissues, we introduced a transfer index that represents the product of tissue-blood ratio of Gd-DTPA and the ratio of extracellular volume of a tissue based on the above findings. The index depends neither on dose of the compound nor on Larmor frequency. The clinical significance of the index was studied in patients with brain tumors. The indexes varied from 0.038 to 0.51, depending on the biological characteristics of the tumors. The transfer index may be used in the quantitative evaluation of MR relaxation enhancement, which may be applied to monitoring therapeutic efficacy and to estimating tissue perfusion.

Brain↗
PubMed1985

Enhanced expression in vivo of HLA-ABC antigens and beta 2-microglobulin on human lymphoid cells induced by human interferon-alpha in patients with lung cancer. Enhanced expression of class I major histocompatibility antigens prior to treatment.

The effect of cloned human interferon-alpha (IFN-alpha) on the expression of HLA-ABC antigens (HLA-ABC) and beta 2-microglobulin (beta 2m) on human peripheral lymphoid cells in vivo was studied by cytofluorometry using monoclonal antibodies and fluorescein-labelled rabbit anti-mouse immunoglobulin. A significant increase in the mean fluorescence intensity of HLA-ABC (median 59%, P less than 0.001) and beta 2m (median 57%, P less than 0.001) on small lymphoid cells was observed 24 h after initiation of IFN-alpha treatment (50 X 10(6) units IFN-alpha/m2 three times a week). The enhanced expression of these antigens in vivo was found in 11 of 12 examined patients with primary bronchial carcinoma. A concomitant increase in serum beta 2m (median 90%, P less than 0.001) was found in all patients. In contrast the amount of cell-associated HLA-ABC and beta 2m remained unchanged (P greater than 0.1 and P greater than 0.5, respectively) by day-to-day analysis of an untreated healthy control group. An increased expression of both HLA-ABC (mean 55%, P less than 0.0005) and beta 2m (mean 23%, P less than 0.01) was also observed prior to treatment in the lung cancer patients when compared to a group of age matched healthy individuals. Treatment with IFN-alpha caused a significant redistribution of mononuclear cells resulting in both absolute and relative lymphopenia. Pre-treatment lymphocyte counts were 1.09 X 10(9)/1 (range 0.49-1.73), post-treatment counts were 0.55 X 10(9)/1 (range 0.39-1.06).

Adult↗
PubMed1988

Enhanced activity of murine peritoneal cells after aclacinomycin injection: characteristics of the enhanced respiratory burst.

After the i.p. injection into normal mice, of 4 mg/kg of aclacinomycin (ACM), a dose which prolongs the survival of tumor-bearing mice, the zymosan-elicited chemoluminescence (CL) of the peritoneal cells (PC) is greater than that of control cells. The volume in which the drug is administered plays an important role in the intensity of the response. ACM also stimulated the CL of PC from tumor-bearing mice. It is known that CL can also be elicited by soluble stimuli such as 4 beta-phorbol-12-myristate-13 alpha-acetate or Ca2+ ionophore A 23187, which, however, act in different ways. The response of ACM cells to these stimuli is also greater than in control cells. The enhanced CL of ACM-treated cells can be inhibited by incubating in vitro the zymosan-triggered PC with superoxide dismutase (300 units/ml) and catalase (2750 units/ml), but not with ethanol (20 microM) or potassium cyanide (100 microM). This indicates the participation of O2- and H2O2 in the CL of ACM-treated cells, whereas mitochondrial respiration does not appear to be involved. Furthermore, the following facts suggest the participation of arachidonic acid metabolism in the control of CL: (a) the in vitro addition of nordihydroguaiaretic acid (7 x 10(-6) M) and indomethacin (10(-3) M) inhibits the CL, while indomethacin (10(-6) M) has the opposite effect; (b) the PC from normal or ACM-treated mice when stimulated with zymosan secrete high amounts of prostaglandin (PG); (c) treated cells secrete the same amounts of PGE2 and 6-keto-PGF1 alpha but the secretion of PGF2 alpha and particularly of thromboxane B2 is greater in treated cells than in control cells and indomethacin (10(-6) M) strongly inhibits PG secretion in all groups; (d) in vitro addition of PGE2 at a concentration of 10(-6) M has an inhibitory effect on the CL emission of control and of treated cells, but it does not have this effect at lower concentrations (10(-8) M). These data suggest that the lipoxygenase pathway of arachidonic acid metabolism may be involved in the triggering of CL of ACM-treated cells, as well as that of normal cells, whereas products of the cyclooxygenase pathway may act as feedback inhibitors.

Aclarubicin↗
PubMedDate not supplied

Salt sensitivity in humans is linked to enhanced sympathetic responsiveness and to enhanced proximal tubular reabsorption.

If high sodium intake is involved in the pathogenesis of essential hypertension, the effects of changing the sodium intake should be demonstrable in the susceptible part of the normotensive population. Therefore, we have investigated the effects of moderate salt restriction in 52 young normotensive subjects with and without a family history of hypertension; 22 (42%) responded to moderate salt restriction (200 to 50 mmol/day) over 2 weeks, with a significant fall in blood pressure shown by continuous automatic blood pressure recordings. Accordingly, these subjects were classified as salt-sensitive, and the remainder as salt-resistant. Compared to salt-resistant subjects, salt-sensitive subjects showed a 2.5-fold higher incidence of a positive family history of hypertension (p less than 0.01), and a significantly higher blood pressure and lower salivary sodium concentration during the usual high sodium diet. Although there were no differences in Na,K-ATPase activity and in Na-K cotransport of erythrocytes, the pressor response to infused norepinephrine in salt-sensitive subjects was double that of salt-resistant subjects independent of the diet and this was linked to indirect evidence for enhanced proximal tubular sodium reabsorption. On the usual high sodium diet, 40% of the normal population may be salt-sensitive and prone to develop hypertension. Hypersensitivity to catecholamines (genetically determined?) may be the cause of salt sensitivity. A low sodium concentration in saliva deserves further study as a simple screening test to identify salt-sensitive subjects.

Adult↗
PubMed1993

Retinoic acid enhances fibrinolytic activity in-vivo by enhancing tissue type plasminogen activator (t-PA) activity and inhibits venous thrombosis.

We studied the profibrinolytic effect and the anti-thrombotic potential of retinoic acid in-vivo. Male Wistar rats were treated with retinoic acid either acutely or twice daily for a period of 5 consecutive days in a dose range of 0.01 to 3.0 mg/kg. Fibrinolytic activity was measured ex-vivo using the diluted blood clot lysis test and net t-PA activity in tissue extracts was measured in a spectrophotometric rate assay. Clot lysis was dose dependently increased by retinoic acid up to about 170% (relative to vehicle treated rats) at a dose of 3 mg/kg. No tachyphylaxis could be detected. Ex-vivo measured fibrinolytic activity after single administration of 1 mg/kg of retinoic acid peaked at 3 h after ingestion. Even after 18 h a significantly higher clot lysis rate was measured. Lysis of blood clots from vehicle and retinoic acid treated rats could be completely blocked by addition of tranexamic acid or antibodies against rat t-PA before clot formation. t-PA activity in plasma was slightly increased after retinoic acid treatment; no effects were measured on plasma PAI-1, u-PA, plasminogen, and alpha 2-antiplasmin levels. t-PA activity in lung and kidney was marginally enhanced by retinoic acid but in heart and aortic tissue extracts t-PA activity was increased by about 50%. We confirmed this potential anti-thrombotic property in an in-vivo venous thrombosis model. A reduced clot size was observed after retinoic acid administration (35% reduction at a dose of 1 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Enhanced levels and enhanced clonogenic capacity of blood progenitor cells following administration of stem cell factor plus granulocyte colony-stimulating factor to humans.

Administration of hematopoietic growth factors is being used increasingly to obtain populations of blood progenitor/stem cells (PBPC) for clinical transplantation. Here we examined the effect of combining stem cell factor (SCF ) and granulocyte colony-stimulating factor (G-CSF ) versus G-CSF alone in a randomized clinical study involving 62 women with early-stage breast cancer. In the first patient cohorts, escalating doses of SCF were administered for 7 days with concurrent G-CSF administration. At baseline, levels of progenitor cells in the bone marrow or blood were comparable in the different patient groups. As with administration of G-CSF alone, the combination of SCF plus G-CSF did not alter the wide variation in levels of PBPC observed between individuals and did not alter the selective nature of PBPC release, with preferential release of day-14 granulocyte-macrophage colony-stimulating factor (GM-CFC) versus day-7 GM-CFC. However, SCF acted to sustain the levels of PBPC after cessation of growth factor treatment; levels of PBPC were elevated 100-fold at later timepoints compared with G-CSF alone. In addition, the maximum levels of PBPC observed were increased approximately fivefold at day 5 of growth-factor administration. The increased levels of PBPC resulted in significantly increased levels of PBPC obtained by leukapheresis. In a subsequent patient cohort, 3-days pretreatment with SCF was introduced and followed by 7 days concurrent SCF plus G-CSF. The 3-days pretreatment with SCF resulted in an earlier wave of PBPC release in response to commencement of G-CSF. In addition, maximum PBPC levels in blood and PBPC yield in leukapheresis products were further increased. Unexpectedly however, SCF pretreatment resulted in progenitor cells with enhanced self-generation potential. Recloning assays documented the ability of approximately 30% of primary granulocyte-macrophage (GM) colonies from control cell populations to generate secondary GM colonies (n = 1,106 primary colonies examined). In contrast approximately 90% of GM colonies from PBPC after SCF pretreatment generated secondary clones and 65% generated secondary colonies. The action of SCF was not explicable in terms of altered SCF, GM-CSF, or G-CSF responsiveness, but SCF pretreatment was associated with maximum serum SCF levels at the time G-CSF was commenced. These results show that PBPC populations mobilized by different growth factor regimens can differ in their functional properties and caution against solely considering number of harvested progenitor cells without regard to their function.

Administration, Cutaneous↗
PubMed1998

Type I interferon induces inhibitory 16-kD CCAAT/ enhancer binding protein (C/EBP)beta, repressing the HIV-1 long terminal repeat in macrophages: pulmonary tuberculosis alters C/EBP expression, enhancing HIV-1 replication.

We have previously observed that HIV-1 replication is suppressed in uninflamed lung and increased during tuberculosis. In vitro THP-1 cell-derived macrophages inhibited HIV-1 replication after infection with Mycobacterium tuberculosis. Suppression of HIV-1 replication was associated with inhibition of the HIV-1 long terminal repeat (LTR) and induction of ISGF-3, a type I interferon (IFN)-specific transcription factor. Repression of the HIV-1 LTR required intact CCAAT/enhancer binding protein (C/EBP) sites. THP-1 cell-derived macrophages infected with M. tuberculosis, lipopolysaccharide, or IFN-beta induced the 16-kD inhibitory C/EBPbeta isoform and coincidentally repressed HIV-1 LTR transcription. C/EBPbeta was the predominant C/EBP family member produced in THP-1 macrophages during HIV-1 LTR repression. In vivo, alveolar macrophages from uninflamed lung strongly expressed inhibitory 16-kD C/EBPbeta, but pulmonary tuberculosis abolished inhibitory C/EBPbeta expression and induced a novel C/EBP DNA binding protein. Therefore, in vitro, proinflammatory stimulation produces an IFN response inhibiting viral replication by induction of a C/EBPbeta transcriptional repressor. THP-1 cell-derived macrophages stimulated with type I IFN are similar to alveolar macrophages in the uninflamed lung in vivo. In contrast, the cellular immune response in active pulmonary tuberculosis disrupts this innate immunity, switching C/EBP expression and allowing high level viral replication.

Base Sequence↗
PubMed1998

Differences in predominant enhancement mechanisms of superparamagnetic iron oxide and ultrasmall superparamagnetic iron oxide for contrast-enhanced portal magnetic resonance angiography. Preliminary results of an animal study original investigation.

RATIONALE AND OBJECTIVES: To determine the effect of particle size of superparamagnetic iron oxide (SPIO) contrast agents on magnetic resonance angiography of the portal venous system. METHODS: We studied eight beagle dogs by a T1-weighted 3D turbo-gradient echo magnetic resonance (MR) angiography sequence (TE 4 milliseconds, TR 11 milliseconds, flip angle 25 degrees, coronal imaging plane) before and after administration of either Resovist (SHU555A), a superparamagnetic iron oxide contrast agent with a mean particle size of 60 nm and a relaxivity ratio R2/R1 of approximately 7, or a new ultrasmall superparamagnetic iron oxide (USPIO) contrast agent with a mean particle size of approximately 20 nm and a R2/R1 ratio of approximately 2. Images were acquired on a 1.5-T MR body scanner. Both agents were injected as a peripheral bolus of 40 mumol Fe/kg body weight. Repeated scans were acquired before, immediately after, and 10, 20, 30, and 40 minutes after administration of the agent. RESULTS: After administration of Resovist, portal venous signal increased to 237% of control immediately after injection, while hepatic parenchymal signal intensity decreased to 86% of control. The maximal CNR increase to 177% was achieved immediately after injection of the agent. After USPIO, portal venous signal increased to 401% of the precontrast value immediately after injection, while hepatic parenchymal signal intensity also increased to 131% of control at this time. Hepatic signal then decreased progressively to 49% of control after 40 minutes. The maximal CNR increase to 326% was achieved 10 minutes after injection of the agent. CONCLUSIONS: It is concluded that superparamagnetic iron oxide particles of different sizes have different R2/R1 ratios and, consequently, different mechanisms of contrast improvement in T1-weighted portal MR angiograms.

Animals↗
PubMed2000

An intronic splicing enhancer binds U1 snRNPs to enhance splicing and select 5' splice sites.

Intronic G triplets are frequently located adjacent to 5' splice sites in vertebrate pre-mRNAs and have been correlated with splicing efficiency and specificity via a mechanism that activates upstream 5' splice sites in exons containing duplicated sites (26). Using an intron dependent upon G triplets for maximal activity and 5' splice site specificity, we determined that these elements bind U1 snRNPs via base pairing with U1 RNA. This interaction is novel in that it uses nucleotides 8 to 10 of U1 RNA and is independent of nucleotides 1 to 7. In vivo functionality of base pairing was documented by restoring activity and specificity to mutated G triplets through compensating U1 RNA mutations. We suggest that the G-rich region near vertebrate 5' splice sites promotes accurate splice site recognition by recruiting the U1 snRNP.

Base Pairing↗