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Biomedical subjects

M M Reddy

Publications and source records attributed to M M Reddy.

At least 73 records · Page 4Linked to original sources
PubMed1989

Elevated soluble CD8 levels in sera of human immunodeficiency virus-infected populations.

Soluble CD8 levels in sera were quantitated in asymptomatic intravenous drug abusers, homosexuals, and patients with lymphadenopathy or acquired immunodeficiency syndrome. Soluble CD8 levels were elevated in human immunodeficiency virus-seronegative intravenous drug abusers and homosexuals, probably reflecting infections like cytomegalovirus. The sera of human immunodeficiency virus-seropositive groups of patients with human immunodeficiency virus infection also had elevated levels of soluble CD8, reflecting infections like cytomegalovirus and human immunodeficiency virus infection.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Neopterin and alpha and beta interleukin-1 levels in sera of patients with human immunodeficiency virus infection.

Levels of neopterin and alpha and beta interleukin-1 (IL-1) in sera of normal controls, asymptomatic intravenous drug abusers, homosexuals, and patients with lymphadenopathy or acquired immunodeficiency syndrome were measured. Neopterin levels were elevated in the sera of human immunodeficiency virus (HIV)-seronegative intravenous drug abusers and homosexuals, as well as in the sera of HIV-seropositive patients. Alpha IL-1 was the most predominant form of IL-1 found in the sera of all groups, and its level in HIV-seronegative intravenous drug abusers was elevated compared with the level in controls, whereas its levels in asymptomatic HIV-seropositive intravenous drug abusers and asymptomatic HIV-seronegative and HIV-seropositive homosexuals were decreased relative to the level in controls. Beta IL-1 levels in sera in all groups were not significantly different from the control value, except for the HIV-seropositive homosexual group; in this group the beta IL-1 level was significantly decreased compared with the control value.

AIDS-Related Complex↗
PubMed1989

Altered electrical potential profile of human reabsorptive sweat duct cells in cystic fibrosis.

The electrophysiological properties of reabsorptive sweat duct (RSD) cells from normal and cystic fibrosis (CF) subjects were studied using intracellular microelectrodes. The apical membrane potential (Va) of CF duct cells was reversed in "polarity" (+28.0 +/- 2.4 mV, n = 46) compared with normal duct cells (-24.9 +/- 0.4 mV, n = 145), and the basolateral membrane potential (Vb) of CF cells was hyperpolarized significantly (-50.1 +/- 1.2 mV, n = 46) in comparison to normal cells (-34.6 +/- 0.4 mV, n = 145). The substitution of the impermeant anion gluconate for Cl- in the lumen of the normal duct depolarized Va from -24.9 +/- 1.1 to 8.9 +/- 3.1 mV (n = 18) and hyperpolarized Vb from -34.3 +/- 1.1 to -55.6 +/- 3.7 mV (n = 18), which mimicked the cell electrical potential profile of CF ducts even in the presence of Cl-. Cl- substitution in the bath depolarized Vb of normal ducts by 22.5 +/- 2.6 mV (n = 24), while hyperpolarizing Va by -3.4 +/- 1.6 mV (n = 24). The response of the electrical profiles of CF cells to Cl- substitution in either the lumen or the bath was significantly reduced compared with normal cells. The effect of the Na+ conductance blocker amiloride (10(-4) M) on Vb was not significantly different in CF (delta Vb = -26.4 +/- 3.8 mV, n = 9) vs. normal (delta Vb = -27.6 +/- 2.5 mV, n = 30) cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Localization of Cl- conductance in normal and Cl- impermeability in cystic fibrosis sweat duct epithelium.

We studied the Cl- permeability properties of apical and basolateral membranes of human reabsorptive sweat duct (RSD) from normal and cystic fibrosis (CF) subjects. In normal ducts, Cl- substitution by impermeant anion gluconate in the lumen increased the voltage divider ratio (VDR) from 4.8 +/- 0.9 to 7.0 +/- 1.1 (n = 8, P less than 0.05), whereas Cl- substitution in the contraluminal bath decreased the VDR from 3.2 +/- 0.7 to 1.9 +/- 0.4 (n = 7, P less than 0.05). These results are consistent with a significant Cl- permeability in both apical and basolateral membranes of normal ducts. Amiloride (10(-4) M) in the lumen of normal ducts resulted in a small increase in VDR from 4.2 +/- 0.6 to 5.0 +/- 0.8 (n = 10, P less than 0.05), whereas the current-induced basolateral membrane voltage deflections (delta Vb) increased from 6.9 +/- 1.3 to 7.7 +/- 1.2 mV, suggesting that inhibition of Na+ permeability decreased basolateral membrane Cl- permeability. In the absence of luminal Cl-, amiloride decreased delta Vb and induced much greater effect on VDR (from 5.2 +/- 1.1 to 10.8 +/- 2.3, n = 9, P less than 0.05) than in the presence of Cl-. Likewise, in the presence of amiloride, Cl- substitution in the lumen had greater effect on VDR (increased from 3.5 +/- 0.5 0.5 to 10.0 +/- 1.5, n = 15, P less than 0.05) than in the absence of amiloride. These results indicate that Na+ conductance in the apical membrane of the normal duct is significantly smaller than Cl- conductance.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1988

Retention of basic electrophysiologic properties by human sweat duct cells in primary culture.

The present investigation was undertaken to examine the usefulness of cultured human sweat duct cells for ion transport and related studies in the genetic disease, cystic fibrosis. Electrical properties of cultured duct (CD) cells were compared with electrical properties of microperfused duct (MPD) cells. The resting apical membrane potential (Va) of the CD cells was -26.4 +/- 0.9 mV, n = 158 cells as compared to -24.3 +/- 0.6 mV, n = 105 of MPD cells. The Na+-K+ pump inhibitor ouabain, when applied to the apical surface of the CD cells and basolateral surface of MPD cells, depolarized both CD cells (from -28.6 +/- 3.6 to -16.8 +/- 2.4 mV, n = 5) and MPD cells (from -23.8 +/- 0.5 mV to -19.5 +/- 1.8 mV, n = 6). The Na+ conductance inhibitor amiloride applied to the apical surface hyperpolarized the apical membrane potentials (Va) of CD cells and MPD cells by -13.2 +/- 1.4 mV, n = 43 and -34.3 +/- 3.1 mV, n = 19), respectively, indicating the presence of amiloride sensitive Na+ channels in both groups of cells. However, the amiloride sensitivity of CD cells was dependent on the age of the culture. Cl- substitution at the apical side by the impermeant anion gluconate depolarized the Va of CD cells and MPD cells by 12.2 +/- 0.9 mV, n = 32 and 37.9 +/- 4.3 mV, n = 12, respectively. The effect of beta-adrenergic agonist isoproterenol (IPR), was inconsistent. In CD cells, IPR either hyperpolarized (delta Va = -8.3 +/- 1.2 mV, n = 5) or depolarized (delta Va = 8.2 +/- 2.3 mV, n = 4) or had no effect, n = 2. In contrast, most of the MPD cells did not respond to IPR, but three cells had a varied response to IPR. Our results suggest that CD cells, like MPD cells, retain significant Na+ and Cl- conductances. CD cells seem to have developed a higher sensitivity to beta-adrenergic stimulation in tissue culture as compared to MPD cells.

Amiloride↗
PubMed1988

Open study of AL-721 treatment of HIV-infected subjects with generalized lymphadenopathy syndrome: an eight week open trial and follow-up.

AL-721 is a lipid compound composed of neutral lipids, phosphatidylcholine and phosphatidylethanolamine in a 7:2:1 ratio. The objective of this open study was to evaluate the effects of AL-721 in vivo in an 8-week open trial in which 10 g twice daily was administered on a low fat diet to eight HIV-infected subjects with lymphadenopathy syndrome (LAS). Serial lymphocyte cocultivation studies in 7 patients with initial culture positivity appeared to demonstrate reduction of reverse transcriptase peak counts in 5 with the trough noted in 4 at 8 weeks and in one at 4 weeks following termination of therapy. The mean values for all 7 patients revealed a baseline value of 73,419 with decrease to a low of 27418 at 8 weeks. Mean levels of total lymphocytes, T-4, T-8 and T-11 cells were not altered but lymphoproliferative responses to concanavalin A and pokeweed mitogens appeared to be augmented in 4 of the 8 subjects in association with AL-721 treatment. No side effects were noted. In a subsequent follow-up study using a normal diet in the same subjects lymphocyte cocultivation and mitogen-induced responses were less consistently affected when 15 g twice daily AL-721 was readministered. In addition, serum HIV p24 antigen and CD4 levels were not altered during both the 8-week open and subsequent AL-721 readministration. Four of the 8 patients have progressed to AIDS over the subsequent 14 months.

AIDS-Related Complex↗
PubMed1988

Elevated soluble interleukin-2 receptor levels in serum of human immunodeficiency virus infected populations.

Soluble interleukin-2 receptor (SIL-2R) levels in sera were quantitated in asymptomatic intravenous drug abusers (IVDA) and in patients with lymphadenopathy or AIDS. The mean SIL-2R level in serum of normal controls was 158 +/- 19 compared to 368 +/- 35 U/ml in serum of HIV-seronegative asymptomatic IVDA. The mean SIL-2R in serum of HIV-seropositive asymptomatic IVDA was 609 +/- 85 U/ml and in patients with lymphadenopathy was 745 +/- 79 U/ml. In addition, AIDS patients with Pneumocystis carinii pneumonia, Kaposi's sarcoma, or both had elevated mean levels of SIL-2R values with a broad range. This elevated level of SIL-2R may reflect excessive cell surface IL-2R expansion by the infected cells.

AIDS-Related Complex↗
PubMed1988

Tumor necrosis factor and HIV P24 antigen levels in serum of HIV-infected populations.

Tumor necrosis factor (TNF) and HIV P24 antigen levels were determined in the serum of intravenous drug abusers (IVDAs), homosexuals, and patients with lymphadenopathy or acquired immune deficiency syndrome (AIDS). The mean TNF level in the serum of normal controls was 12 +/- 5 compared to 112 +/- 25 pg/ml in the serum of HIV-seronegative asymptomatic IVDAs. This increase of TNF may be due to the variety of infections that these people are exposed to persistently. The mean TNF level in the serum of HIV-seropositive asymptomatic IVDAs was 112 +/- 79 pg/ml, 31 +/- 24 pg/ml in lymphadenopathy, and 55 +/- 19 pg/ml in patients with AIDS. The mean P24 level in the serum of patients with AIDS was 50 +/- 13 pg/ml compared to 0 pg/ml in HIV-seronegative subjects, while the other HIV-seropositive groups had relatively low levels. The P24 antigen levels may reflect viral load in these patients. SIL-2R and beta2-microglobulin levels were also elevated in patients with HIV infection . The TNF may play a role in the antiviral activity against HIV virus and in the development of full-blown disease after HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Intracellular potentials of microperfused human sweat duct cells.

Intracellular potentials of cells from isolated segments of microperfused human sweat ducts were measured in order to determine the electrical profiles of these cells under resting, transporting, and inhibited conditions. Even though the cells are relatively small (ca. 6-8 microns), continuous recordings of intracellular potentials from the same impalement were stable for up to 2 h. In the resting condition in normal Ringer's solution when the lumen of the duct was collapsed and not perfused, the intracellular potential measured across the basal membrane was 34.6 +/- 1.5 mV (n = 31; mean +/- SE). In the same bathing medium, when the duct lumen was also perfused with normal Ringer's solution, the basolateral membrane potential (Vb), the apical membrane potential (Va) and transepithelial potential (Vt) was -33.8 +/- 0.47 mV, -23.7 +/- 0.48 mV and -9.6 +/- 0.9 mV (n = 73), respectively. The average input impedence (Ri) of these cells was 19.6 +/- 0.4 M omega (n = 36). The frequency distribution of Vb was unimodal suggesting that only one functional cell type exists in this tissue. Amiloride (0.1 mM) in the lumen hyperpolarized both Va and Vb by -40.5 +/- 3.6 mV and -33.2 +/- 3.7 mV (n = 15), respectively, with a slight but significant increase in Ri(15%) while abolishing Vt. Removing luminal Cl- depolarized Va by +37.0 +/- 4.2 mV and hyperpolarized Vb by -19.0 +/- 4.2 mV (n = 11). Removing Cl- from the bath hyperpolarized Va by -3.3 +/- 2.3 mV and depolarized Vb by +24.3 +/- 2.7 mV (n = 15).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1987

In vitro immunomodulatory effects of interleukin-2 and thymosin fraction V in acquired immune deficiency syndrome.

A monoclonal antibody (anti-Tac) that appears to bind the receptor for interleukin-2 (IL-2) was used to quantitate lymphocytes that express IL-2 receptors (IL-2R) in response to phytohemagglutinin (PHA) stimulation. 62 +/- 4% of the cells expressed IL-2R in response to PHA in twelve normal subjects compared to 22 +/- 4% in fourteen patients with acquired immune deficiency syndrome (AIDS) (P less than 0.001) and 50 +/- 6% in six patients with AIDS-related complex (P less than 0.1). There was no effect on IL-2R expression, when lymphocytes from seven controls were incubated with IL-2 (20 mu/ml) or thymosin fraction V (10 mu/ml) for 72 h. However, when the lymphocytes from seven patients with AIDS were incubated with IL-2, the IL-2R rose from 18 +/- 3% to 31 +/- 3% (P less than 0.005) and with a fraction V to 29 +/- 3% (P less than 0.001). In addition, IL-2 augmented the PHA-induced proliferative responses in patients with AIDS-related complex and AIDS and normal controls, whereas thymosin fraction V had no significant effect. Thymosin fraction V also enhanced the IL-2 production of PHA-stimulated mononuclear cells obtained from six patients with AIDS and six normal controls. These results suggest that both IL-2 and thymosin fraction V can modulate in vitro T-cell function in patients with AIDS.

AIDS-Related Complex↗
PubMed1987

Effect of dieldrin on catalytic potential of field mouse Mus booduga brain acetylcholinesterase.

Substrate kinetics of acetylcholinesterase (AChE) were investigated in control and dieldrin-treated Mus booduga brains. Non competitive inhibition with respect to activation by acetylcholine was indicated by decreased maximal velocity (V) without change in Michaelis-Menten constant (Km). Activation energies (delta E) were found to be increased suggesting decreased efficiency of enzyme in dieldrin-treated mouse brains. Fall in the activity potential of AChE may account for the interference of dieldrin or its metabolites with the acetylcholine (ACh)--AChE system and deserve consideration in contributing to the neurotoxicity.

Acetylcholinesterase↗
PubMed1987

Cl- permeability of sweat duct cell membranes: intracellular microelectrode analysis.

Cl- permeability in the reabsorptive sweat duct (RSD) epithelium from normal subjects was studied using electrophysiological techniques. The average basolateral membrane potential (Vb) of normal ducts was -36.8 +/- 0.8 mV and the average apical membrane potential (Va) was -27.2 +/- 0.8 mV (n = 45). Amiloride in the lumen of microperfused sweat ducts hyperpolarized Va by 34.3 +/- 3.1 mV and Vb by 25.7 +/- 3.1 mV (n = 12) with a small but significant increase in voltage divider ratio (Ra/Rb) from 4.2 +/- 0.8 to 5.0 +/- 0.8 (n = 8). Cl- substitution in the lumen depolarized Va by +37 +/- 4.2 (n = 11) accompanied by a significantly larger increase in Ra/Rb from 4.8 +/- 2.6 (n = 8) to 7.0 +/- 3.1 (n = 8). Bath Cl- substitution depolarized Vb by +24.3 +/- 2.7 mV (n = 15) while decreasing Ra/Rb from 3.2 +/- 0.7 to 1.9 +/- 0.4 (n = 7). These results indicated a significant Cl- permeability in both apical and basolateral membranes. Removing Cl- from the lumen significantly decoupled Va and Vb and restricted the amiloride-induced hyperpolarization to the apical membrane. This result may suggest that intracellular Cl- might be responsible for coupling Va and Vb and that hyperpolarization of Va and Vb by amiloride may result in changes in intracellular Cl-. Alternatively, Va and Vb could be coupled through a Cl- sensitive paracellular shunt. These results are consistent with Cl- permeability in both apical and basolateral membranes of duct cells. However, the question of whether paracellular Cl- permeability is important in Cl- uptake cannot be determined from the present data.

Amiloride↗
PubMed1987

Effects of bumetanide on chloride transport in human eccrine sweat ducts: implications for cystic fibrosis.

The effect of the loop diuretic bumetanide on Cl- transport in the human reabsorptive sweat duct (RSD) was studied to determine the properties of Cl- transport in this tissue with an emphasis on its role in cystic fibrosis. Bumetanide (10(-4) M) in the bath decreased the NaCl reabsorption rate (+/- SE) from 235 +/- 72 to 77 +/- 24 pmol/min per mm (n = 10). Bumetanide in the lumen decreased the rate of NaCl reabsorption to a lesser extent from 132 +/- 17 to 84 +/- 16 pmol/min per mm (n = 9). At least part of this inhibition appears to be due to the inhibition of a Cl- conductance in the RSD, as evidenced by a significant increase in the specific resistance (Rt) of the tissue from 8.3 +/- 0.6 to 52.7 +/- 19.3 omega/cm2(n = 3) due to bumetanide in the bath. Luminal bumetanide also increased Rt but to a lesser degree [from 9.8 +/- 1.2 to 16.4 +/- 2.0 omega/cm2 (n = 3)]. Bumetanide also affected the transepithelial potential (Vt), hyperpolarizing it from -10.9 +/- 0.8 to -28.6 +/- 2.0 mV (n = 13). In ouabain-inhibited ducts, a threefold dilution of luminal NaCl concentration resulted in a -13.5 +/- 1.7 mV dilution diffusion potential which was abolished by bumetanide in the bath, indicating that bumetanide removed the anion selectivity of the epithelium. Bumetanide hyperpolarized the basolateral membrane potential (Vb) from -33.6 +/- 1.9 to -44.3 +/- 1.4 mV and depolarized the apical membrane potential (Va) from -20.9 +/- 0.9 to 14.0 +/- 1.3 mV. These results suggest that bumetanide inhibits transcellular Cl- conductance with possible additional effects on the paracellular Cl- conductance pathway as well.

Absorption↗
PubMed1985

Augmentation of mitogen-induced proliferative responses by in vitro indomethacin in patients with acquired immune deficiency syndrome and AIDS-related complex.

The effect of indomethacin on mitogen-induced lymphocyte proliferative responses was studied in six normal heterosexual subjects and nine patients with the acquired immune deficiency syndrome (AIDS) and AIDS-related complex (ARC). Indomethacin enhanced only Con A-induced lymphocyte responses in six heterosexual men. In contrast, study of the cells from AIDS and ARC revealed that indomethacin enhanced PHA-induced lymphocyte proliferative responses from 52,600 counts/min to 70,900 counts/min (P less than 0.005) and 81,400 counts/min (P less than 0.001) at 0.1 and 1 microgram/ml. respectively and increased Con A-induced lymphoproliferation from 30,800 counts/min to 52,000 counts/min (P less than 0.01) at 0.1 microgram/mg and 51,1000 counts/min (P less than 0.005) at 1 microgram/ml. These results suggest that indomethacin enhanced mitogen-induced lymphoproliferative responses in vitro with cells from patients with AIDS and AIDS-related complex and may have therapeutic potential in some patients with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Elevated beta 2-microglobulin and lysozyme levels in patients with acquired immune deficiency syndrome.

beta 2-Microglobulin (beta 2-M) levels in sera and urines, and lysozyme levels in sera, were quantitated in healthy heterosexual men and several groups of homosexual males. The mean beta 2-M levels in sera and urines and lysozyme levels in sera of healthy heterosexual and homosexual men were not significantly different. However, beta 2-M levels in patients with lymphadenopathy syndrome and AIDS were elevated. The mean beta 2-M level in sera of 11 patients with the lymphadenopathy syndrome was 4016 +/- 473 micrograms/l (SEM) (P less than 0.001) and 5409 +/- 462 micrograms/l (P less than 0.001) in 27 patients with AIDS. Similarly, beta 2-M levels in the urines of patients with chronic diarrheal syndrome, lymphadenopathy syndrome, and those meeting the CDC surveillance definition of AIDS were also significantly elevated (P less than 0.025). The mean lysozyme levels in the sera of 11 patients with the lymphadenopathy syndrome was 16.58 +/- 0.04 microgram/ml, and in 27 patients with AIDS 15.40 +/- 1.16 microgram/ml, compared to the mean level obtained in normal heterosexual men of 6.67 +/- 0.42 microgram/ml (P less than 0.001). The results of this study suggest that measuring beta 2-M in serum and urine and lysozyme levels in serum might provide additional useful parameters for the evaluation of patients with AIDS and prodromal syndromes.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Different types of potassium transport linked to carbachol and gamma-aminobutyric acid actions in rat sympathetic neurons.

Carbachol and gamma-aminobutyric acid depolarize mammalian sympathetic neurons and increase the free extracellular K+-concentration. We have used double-barrelled ion-sensitive microelectrodes to determine changes of the membrane potential and of the free intracellular Na+-, K+- and Cl- -concentrations ( [Na+]i, [K+]i and [Cl-]i) during neurotransmitter application. Experiments were performed on isolated, desheathed superior cervical ganglia of the rat, maintained in Krebs solution at 30 degrees C. Application of carbachol resulted in a membrane depolarization accompanied by an increase of [Na+]i, a decrease of [K+]i and no change in [Cl-]i. Application of gamma-aminobutyric acid also induced a membrane depolarization which, however, was accompanied by a decrease of [K+]i and [Cl-]i, whereas [Na+]i remained constant. Blockade of the Na+/K+-pump by ouabain completely inhibited both the reuptake of K+ and the extrusion of Na+ after the action of carbachol, and also the post-carbachol undershoot of the free extracellular K+-concentration. On the other hand, in the presence of ouabain, no changes in the kinetics of the reuptake of K+ released during the action of gamma-aminobutyric acid could be observed. Furosemide, a blocker of K+/Cl- -cotransport, inhibited the reuptake of Cl- and K+ after the action of gamma-aminobutyric acid. In summary, the data reveal that rat sympathetic neurons possess, in addition to the Na+/K+-pump, another transport system to regulate free intracellular K+-concentration. This system is possibly a K+/Cl- -cotransport.

Animals↗