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Biomedical subjects

M Ma

Publications and source records attributed to M Ma.

At least 91 records · Page 5Linked to original sources
PubMed1997

Commonly prescribed salt intake in continuous ambulatory peritoneal dialysis patients is too restrictive: results of a double-blind crossover study.

Salt restriction in continuous ambulatory peritoneal dialysis (CAPD) patients is widely prescribed and thereby may reduce quality of life. It is presumed that this has a beneficial effect on BP and reduces the need for hypertonic dialysate. However, this has never been formally evaluated. A double-blind crossover study of placebo versus sodium chloride pills (60 mEq of sodium per day) is presented in 20 stable CAPD patients, 10 of whom were hypertensive. Dietary sodium was quantified throughout the study by 3-d dietary histories and remained unaltered throughout. There was a clinically unimportant but statistically significant rise in BP with added salt: 135/77 to 144/82 (P < 0.05). No rise in BP occurred in the hypertensive patients. Weights, use of hypertonic dialysate, and BP medications remained unaltered throughout the study. In conclusion, 200 mEq of sodium per day, i.e., a normal sodium intake, is easily tolerated in stable CAPD patients, and the recommended sodium intake commonly prescribed is too restrictive.

Aged↗
PubMed1997

Human immunodeficiency virus type 1 Tat protein induces death by apoptosis in primary human neuron cultures.

Neuronal loss in HIV encephalopathy remains a mystery since HIV-1 productively infects macrophage and microglia and only rarely infects neurons in the central nervous system. Apoptosis is a mechanism which may account for the loss of neurons in HIV-1 infected brain. Putative toxic factors that result in neuronal cell death in HIV-1 infection include the regulatory protein Tat, since this protein is known to be released from HIV-1 infected cells. Here we show that Tat induces cell death by apoptosis in cultured human fetal neurons producing characteristic morphological and biochemical features associated with apoptosis. These findings suggest that Tat may play an important role as a secreted, soluble neurotoxin in HIV-1 associated dementia.

Apoptosis↗
PubMed1997

Effect of jiawei shenqi dihuang tang on the content of urinary protein in patients with diabetic nephropathy.

42 cases of diabetic nephropathy (DN) diagnosed as the type of kidney deficiency and blood stasis were treated with Jiawei Shenqi Dihuang Tang. The therapeutic effect demonstrated that various kinds of symptoms and sings were significantly improved. There was significant difference in the qualitative and quantitative examinations of urinary protein between pre- and post-treatment (P < 0.05).

Adult↗
PubMed1997

Does mexiletine have a preferential action (versus healthy myocardium) on the reentrant circuit of ventricular tachycardia?

The preferential action (in diseased versus healthy myocardium) of class 1a antiarrhythmic but not class 1b agents has been demonstrated on the reentrant circuit. This study assessed the effect of mexiletine on the fragmented electrogram at the origin of ventricular tachycardia (VT) associated with underlying heart diseases. In 11 consecutive patients, VT of the same morphology was induced, and entrained with rapid pacing during, before, and after mexiletine. The width of the fragmented electrogram, VT cycle length, and the block cycle length (defined as the longest VT-interrupting paced cycle length during entrainment) were measured before and after mexiletine and the findings compared. The effective refractory period (ERP) was measured at the pacing site (normal myocardium) and at the VT origin. To assess the preferential action of mexiletine, changes in fragmented electrogram were examined in relation to QRS duration (defined as the index of global intraventricular conduction). After mexiletine, VT cycle length, block cycle length, and fragmented electrogram were prolonged significantly. The QRS duration was also prolonged significantly, but this change was significantly smaller than that in VT cycle length or in the width of the fragmented electrogram. There was no significant change in ERP either at the pacing site or at the VT origin. Mexiletine was confirmed to preferentially depress conduction in the diseased myocardium at the VT origin, and this action occurred at a higher rate during VT.

Adult↗
PubMed1997

[The human SRY gene for prenatal diagnosis].

OBJECTIVE: To establish the method for prenatal sex diagnosis of the fetus carrying sex-linked genetic disorder. METHOD: Human SRY gene was amplified by polymerase chain reaction. A 422-bp male specific fragment was obtained. RESULTS: The fragment was identified in 10 men, but unidentified in 10 women. The diagnostic accordance rate of 20 amniotic fluid samples was 100%, 22 of 47 chorionic villi samples were positive. The rate of positive/negative (22/25) was nearly the sex rate of newborn babies. In the meantime, direct-PCR amplification of blood and amniotic fluid was completed. The fragment was shown from 4 microliters to 0.5 microliters of blood and from 2 ml to 0.5 ml of amniotic fluid. CONCLUSION: The results show that fetal sex determination by PCR will be suitable for clinical prenatal diagnosis of sex-linked genetic disorders.

DNA-Binding Proteins↗
PubMed1996

Immunoglobulin G-mediated inflammatory responses develop normally in complement-deficient mice.

The role of complement in immunoglobulin G-triggered inflammation was studied in mice genetically deficient in complement components C3 and C4. Using the reverse passive Arthus reaction and experimental models of immune hemolytic anemia and immune thrombocytopenia, we show that these mice have types II and III inflammatory responses that are indistinguishable from those of wild-type animals. Complement-deficient and wild-type animals exhibit comparable levels of erythrophagocytosis and platelet clearance in response to cytotoxic anti-red blood cell and antiplatelet antibodies. Furthermore, in the reverse passive Arthus reaction, soluble immune complexes induce equivalent levels of hemmorhage, edema, and neutrophillic infiltration in complement-deficient and wild-type animals. In contrast, mice that are genetically deficient in the expression of Fc receptors exhibit grossly diminished reactions by both cytotoxic antibodies and soluble immune complexes. These studies provide strong evidence that the activation of cell-based Fc gamma R receptors, but not complement, are required for antibody-triggered murine inflammatory responses.

Anemia, Hemolytic↗
PubMed1996

Regulation of the B cell response to T-dependent antigens by classical pathway complement.

Mice deficient in complement components C3 (C3 -/-) and C4 (C4 -/-) were found to have a profound defect in their Ab response to a T-dependent Ag (bacteriophage (phi X174). Characterization of the deficient mice demonstrated a diminished level of peanut agglutinin+ germinal centers and a failure in isotype switching despite normal B cell signaling in vitro. The nature of the defect was found to lie at the B cell level, as the T cells were primed in C3- and C4-deficient mice as well as those in wild-type mice. These results, and the finding that the defect could be partly reversed by a 10-fold increase in Ag dose, support the hypothesis that covalent attachment of complement ligands, i.e., C3b and C3d to the Ag-Ab complex, increases its immunogenicity.

Animals↗
PubMed1996

The role of K+ currents in frequency-dependent spike broadening in Aplysia R20 neurons: a dynamic-clamp analysis.

The R20 neurons of Aplysia exhibit frequency-dependent spike broadening. Previously, we had used two-electrode voltage clamp to examine the mechanisms of this spike broadening (Ma and Koester, 1995). We identified three K+ currents that mediate action-potential repolarization: a transient A-type K+ current (I(Adepol)), a delayed rectifier current (IK-V), and a Ca(2+)-sensitive K+ current(IK-CA). A major constraint in that study was the lack of completely selective blockers for I(Adepol) and I(K-V), resulting in an inability to assess directly the effects of their activation and inactivation on spike broadening. In the present study, the dynamic-clamp technique, which employs computer simulation to inject biologically realistic currents into a cell under current-clamp conditions (Sharp et al., 1993a,b), was used either to block I(Adepol) or I(K-V) or to modify their inactivation properties. The data in this paper, together with earlier results, lead to the following hypothesis for the mechanism of spike broadening in the R20 cells. As the spike train progresses, the primary responsibility for spike repolarization gradually shifts from I(Adepol) to I(K-V) to I(K-Ca). This sequence can be explained on the basis of the relative rates of activation and inactivation of each current with respect to the constantly changing spike durations, the cumulative inactivation of I(Adepol) and I(K-V), and the progressive potentiation of I(K-Ca). Positive feedback interactions between spike broadening and inactivation contribute to the cumulative inactivation of both I(Adepol) and I(K-V). The data also illustrate that when two or more currents have similar driving forces and partially overlapping activation characteristics, selectively blocking one current under current-clamp conditions can lead to a significant underestimate of its normal physiological importance.

Action Potentials↗
PubMed1996

Reperfusion injury of ischemic skeletal muscle is mediated by natural antibody and complement.

Reperfusion of ischemic tissue induces an acute inflammatory response that can result in necrosis and irreversible cell injury to both local vascular endothelium and parenchyma. To examine the pathogenesis of ischemia/reperfusion injury, we have used mice deficient in complement components C3, C4, or serum immunoglobulin in a hindlimb model of ischemia. We found that mice homozygous deficient in C3 or C4 were equally protected against reperfusion injury based on a significant reduction in leakage of radiolabeled albumin out of the vasculature. This demonstrates that classical pathway complement is an important factor in the initiation of inflammation following reperfusion. Furthermore, mice deficient in serum immunoglobulin were equally protected and this protection could be reversed by reconstitution with serum from normal mice. Thus, this report describes a novel mechanism for reperfusion injury that involves antibody deposition and activation of complement leading to inflammation permeability.

Animals↗
PubMed1996

Antibody response to a T-dependent antigen requires B cell expression of complement receptors.

Several lines of evidence indicate that antibody responses to T-dependent antigens require complement receptors expressed on either B lymphocytes or follicular dendritic cells. We have used RAG-2 deficient blastocyst complementation to create mice specifically lacking B cell complement receptors. Despite normal expression of complement receptor 1 (CR1[CD35]) and CR2 (CD21) on follicular dendritic cells, these mice have a profound defect in their capacity to mount a T-dependent antibody response. This is the first direct demonstration in vivo that B cell expression of complement receptors is required for a humoral immune response. This is the first direct demonstration in vivo that B cell expression of complement receptors is required for a humoral immune response. This suggests that CD21 and/or CD35 on B lymphocytes may be required for cellular activation, adsorptive endocytosis of antigen, recruitment to germinal centers, and/or protection from apoptosis during the humoral response to T-dependent antigens.

Animals↗
PubMed1996

Micronuclei induced in round spermatids of mice after stem-cell treatment with chloral hydrate: evaluations with centromeric DNA probes and kinetochore antibodies.

The chromosomal effects of chloral hydrate (CH) on germ cells of male mice were investigated using two methods to detect and characterize spermatid micronuclei (SMN); (a) anti-kinetochore immunofluorescence (SMN-CREST) and (b) multicolor fluorescence in situ hybridization with DNA probes for centromeric DNA and repetitive sequences on chromosome X (SMN-FISH). B6C3F1 mice received single intraperitoneal (i.p.) injections of 82.7, 165.4, or 413.5 mg/kg and round spermatids were sampled at three time intervals representing cells treated in late meiosis, early meiosis, or as spermatogonial stem cells. No increases in the frequencies of SMN were detected for cells treated during meiosis using either SMN-CREST or SMN-FISH methods. After spermatogonial stem-cell treatment, however, elevated frequencies of SMN were detected by both methods. With SMN-FISH, dose trends were observed both in the frequencies of spermatids containing micronuclei and in the frequency of spermatids carrying centromeric label. These findings corroborate the recent report by Allen and colleagues [Allen JW et al.(1994): Mutat. Res. 323:81-88] that CH treatment of spermatogenic stem cells induced SMN. Furthermore, our findings suggest that chromosomal malsegregation or loss may occur in spermatids long after CH treatment of stem cells. Further studies are needed to understand the mechanism of action of the CH effect on stem cells and to determine whether similar effects are induced in human males treated with CH.

Anesthetics, Intravenous↗
PubMed1996

Immunolocalization of the oostatic and prothoracicostatic peptide, Neb-TMOF, in adults of the fleshfly, Neobellieria bullata.

The hexapeptide Neb-TMOF (H-NPTNLH-OH, trypsin modulating oostatic factor of the gray fleshfly, Neobellieria bullata)2 occurs in vitellogenic ovaries and is involved in negative feedback regulation of trypsin biosynthesis in the gut of late vitellogenic females. Polyclonal antisera were raised against the synthetic peptide and were used to identify and immunolocalize Neb-TMOF epitopes in different fleshfly tissues. Neb-TMOF-immunoreactive material first appears in the cortical layer of young vitellogenic oocytes and later spreads over the yolk granules. This suggests a pinocytosis with the three yolk polypeptides (vitellogenins). Controls treated with the preimmune sera or with anti-Neb-TMOF antiserum preadsorbed to Neb-TMOF peptide coupled to a solid phase support did not stain. There was no immunostaining in the central nervous system (brain and ventral nerve cord), the retrocerebral complex, the fat body, or the testes. Western blot analysis showed that the anti-Neb-TMOF antisera specifically recognize a putative hormone precursor polypeptide (Mr 75 kDa) from vitellogenic ovaries. This protein is virtually absent from the hemolymph. It is not immunologically related to the three yolk polypeptides, since it is not recognized by yolk polypeptides antisera. In adult females the ovary appears to be the only site of synthesis of Neb-TMOF and of its precursor. Immunopositive staining is found in the apical areas of ovarian follicle cells, suggesting these cells as a site of hormone precursor biosynthesis. This is the first demonstration that a protein colocalized with yolk proteins might act as a precursor for a folliculostatic hormone.

Animals↗
PubMed1996

Disruption of the Cr2 locus results in a reduction in B-1a cells and in an impaired B cell response to T-dependent antigen.

Covalent attachment of activated products of the third component of complement to antigen enhances its immunogenicity, but the mechanism is not clear. This effect is mediated by specific receptors, mCR1 (CD35) and mCR2 (CD21), expressed primarily on B cells and follicular dendritic cells in mice. To dissect the role of mCR1 and mCR2 in the humoral response, we have disrupted the Cr2 locus to generate mice deficient in both receptors. The deficient mice (Cr2-/-) were found to have a reduction in the CD5+ population of peritoneal B-1 cells, although their serum IgM levels were within the range of normal mice. Moreover, Cr2-/- mice had a severe defect in their humoral response to T-dependent antigens that was characterized by a reduction in serum antibody titers and in the number and size of germinal centers within splenic follicles. Reconstitution of the deficient mice with bone marrow from MHC-matched Cr2+/+ donors corrected the defect, demonstrating that the defect was due to B cells themselves. These results indicate an obligatory role of B cell complement receptors in responses of the B cells to protein antigens.

Animals↗
PubMed1996

Enhanced vasocontraction of rat tail arteries by toxoflavin.

1. It has been suggested that the toxic effect of toxoflavin (TXF) produced by Pseudomonas cocovenenas is mainly due to the impairment of electron transfer of the mitochondrial respiratory chain. However, the cardiovascular effect of TXF is unknown. In the present study, the effect of TXF on the isometric contraction of rat isolated tail artery strips and the underlying mechanisms were investigated. 2. The basal force of the tissues was not affected by the toxin. However, the application of TXF before or during KCl (60 mM) stimulation potentiated KCl-induced vasocontraction, specifically the tonic phase of the contraction. 3. When the vessel strips were precontracted with phenylephrine (Phe), TXF further enhanced the tonic contraction of the tissue. Pretreatment of tissues with TXF also potentiated subsequent vasocontraction induced by Phe. The vasocontractor effects of TXF and Phe, however, were not additive. 4. The vascular effect of TXF was not mediated by oxygen-derived free radicals since catalase and SOD did not affect TXF-enhanced vasocontraction. In contrast, the vasocontractor effect of TXF was dependent on extracellular Ca2+ and abolished by nifedipine (a Ca2+ antagonist). TXF also had no effect on caffeine- or U46619-induced vasocontraction. 5. It is suggested that TXF may potentially contract blood vessels via its effect on Ca2+ channels. This effect of TXF depends on the contractile status of the vascular tissues.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Extracellular human immunodeficiency virus type 1 Tat protein is associated with an increase in both NF-kappa B binding and protein kinase C activity in primary human astrocytes.

Human immunodeficiency virus type 1 (HIV-1) infection has been associated with an increase in the binding of the transcription factor NF-kappa B to its consensus sequence in the viral promoter. Using cultures of primary human fetal astrocytes, we show that exogenous HIV-1 Tat protein, which has been demonstrated to be released from infected cells, is associated with an increase in the binding of this transcription factor to an HIV-1 long terminal repeat kappa B sequence. This effect occurs rapidly and is independent of new protein synthesis. We also demonstrate that extracellular Tat protein is associated with an increase in protein kinase C activity. If Tat functions similarly in other cell types, such findings could relate to some of this protein's previously described physiological effects. These effects include Tat's ability to upregulate the synthesis of specific cytokines and to act as a growth factor.

Antibodies, Viral↗