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Biomedical subjects

M R Escobar

Publications and source records attributed to M R Escobar.

At least 19 recordsLinked to original sources

[The use of transabdominal ultrasound in the estimation of postmicturitional residual urine].

OBJECTIVE: To evaluate the utility and accuracy of transabdominal ultrasound in the estimation of postmicturition residual urine in patients with symptomatic benign prostatic hyperplasia (BPH). METHODS/RESULTS: The postvoid residual urine was evaluated in 50 selected patients with BPH. The mean age was 60 years. The bladder volume was estimated in all patients and ranged from 210-540 ml (average 339.2). After voiding, the amount of urine was measured and ranged from 145-350 ml (average 223.5). Then the postmicturition residual urine was evaluated by ultrasound (range 60-264 ml; average 112.86) and compared with the bladder catheter measurements (range 50-265 ml; average 112.6), which showed a minimum difference of +/- 3.84 ml SD. CONCLUSION: Transabdominal ultrasound is a good alternative in the estimation of postmicturition residual urine.

Abdomen

Use of digitalis glycosides to identify the mechanisms of amantadine transport by renal tubules.

The mechanism(s) for uptake of organic cations by renal cortical tubules was (were) examined further. Renal cortical tubules were purified from rat kidneys by a Percoll gradient centrifugation technique. Bicarbonate buffer (Krebs-Henseleit, KHS) conditions were altered, and chemical modulators were used which affect the activity of the basolateral Na+/K+-ATPase. Renal tubule uptake of the achiral organic cation amantadine was determined. The cardiac glycosides digoxin and acetylstrophanthidin and ouabagenin did not alter amantadine uptake by either proximal or distal tubule fragments in KHS. However, ouabain inhibited proximal tubule amantadine uptake in a dose-dependent manner with lower potency than distal tubule amantadine uptake in KHS. Ouabain did not inhibit amantadine tubule uptake in phosphate buffer. However, inhibition of amantadine uptake by ouabain returned in a time-dependent manner upon addition of bicarbonate to the phosphate buffer. Low extracellular sodium or potassium did not alter amantadine uptake by proximal tubules. Hypokalemic and hypokalemic/ hyponatremic conditions decreased the inhibitory potency of ouabain for amantadine uptake by proximal tubules. For distal tubules, both hyponatremic and hypokalemic conditions, alone and together, decreased the inhibitory potency of ouabain, but did not affect amantadine uptake in the absence of ouabain. Hypochloremic conditions decreased affinity for amantadine uptake by distal, but not proximal tubules. No change in maximal transport capacity for amantadine uptake was observed under hypochloremic conditions for either tubule fragment. These studies challenge the widely accepted concept of Na+/ K+-adenosine triphosphatase activity and maintenance of the basolateral membrane potential as rate-limiting steps for the energy-dependent renal tubule uptake of organic cations. Furthermore, these studies suggest a mechanism for ouabain inhibition of organic cation renal tubule uptake that may not involve the Na+/K+-adenosine triphosphatase and may be possibly bicarbonate-dependent.

Amantadine

Site-selective effect of bicarbonate on amantadine renal transport: quinine-sensitive in proximal vs quinidine-sensitive sites in distal tubules.

The mechanism for bicarbonate enhancement of amantadine (A+) uptake was studied further. A selective modulatory effect of bicarbonate on the stereoselectivity of inhibition of A+ uptake by the stereoisomers, quinine (Q) and quinidine (QD), as reflected by the reversal of potency (Q > QD in KHS vs. QD > Q in phosphate), is reported. Studies were performed in bicarbonate (KHS) and phosphate buffers using purified cortical proximal (PT) and distal tubules (DT) from rat kidneys. Variations of extracellular K+ and Ca++ were used to assess the effect of membrane depolarization and calcium on A+ uptake by the tubules. K+ concentration manipulation (1.5-100 mM) did not change A+ uptake by PT or DT in KHS buffer. High Ca++ (5.0 mM) decreased A+ uptake by PT in KHS (P < .001), whereas in phosphate buffer, both 2.5 and 5.0 mM Ca++ decreased uptake (P < .001). In DT, 0.25 mM Ca++ enhanced A+ uptake (P < .05) in KHS, but 2.5 and 5.0 mM Ca++ decreased it in both buffers. Inhibition studies with Q and QD were performed to characterize the bicarbonate-dependent and bicarbonate-independent A+ transport sites further. Stereoselectivity of inhibition was observed in PT in all buffers used. Potency of Q was higher than QD in KHS but lower than QD in phosphate-buffered PT. QD potency remained unchanged. In phosphate-plus-bicarbonate-buffered PT, the inhibitory potencies for Q and QD increased, with the potency of QD being greater than in KHS (P < .001). For DT, Q and QD were equipotent in all buffers used.(ABSTRACT TRUNCATED AT 250 WORDS)

Amantadine

L(+)- and D(-)-lactate modulate rat renal tubular accumulation of amantadine in the presence and absence of bicarbonate.

The effect of L(+)-, D(-)- and racemic (DL)-lactate on the energy-dependent renal uptake of the achiral organic cation amantadine was determined with purified proximal and distal cortical tubule fragments isolated from rat kidneys. Kinetic parameters for uptake of amantadine were measured, under constant pH, in bicarbonate buffer (Krebs-Henseleit [KHS]), and in lactate buffers (5 mM) with different proportions of the enantiomers. Km for amantadine uptake increased in all lactate buffers compared with KHS for both proximal and distal tubules. Km for uptake in DL-lactate was similar to that in D(-)-lactate for proximal tubules and to L(+)-lactate in distal tubules, but Km in L(+)-lactate was higher than in D(-)-lactate for both tubules. Maximal transport capacity (Vmax) in DL-lactate and mixtures of enantiomers were similar to KHS but higher than in pure L(+)- and D(-)-lactate. In KHS, lactate inhibited energy-dependent amantadine uptake in a biphasic manner. Graded competitive inhibition of amantadine uptake was observed between 1 and 15 mM lactate for both proximal and distal tubules. This first phase (1-15 mM) inhibited 60% of amantadine uptake. The second phase (15-20 mM lactate) showed a much steeper slope and inhibited the remaining amantadine uptake. There were no differences in inhibitory potencies of the lactate enantiomers for either proximal tubules or distal tubules amantadine tubule uptake. Our present studies suggest that L(+)- and D(-)-lactate modulate amantadine transport by interacting directly with the bicarbonate-dependent transport mechanism(s).

Amantadine

Painful gingivitis may be an early sign of infection with the human immunodeficiency virus.

Anecdotal reports have suggested that painful gingivitis may be associated with infection due to the human immunodeficiency virus (HIV). Twenty patients who presented to the emergency department with a chief complaint of gum pain were evaluated for HIV infection, CD4/CD8 T lymphocyte profiles, complete blood cell counts and differentials, and lymphocyte function (response to mitogenic stimulation). Seven of the 20 patients (35%) were seropositive for HIV. Three of the seven HIV-seropositive patients were unaware of their HIV infection until tested in this study (with use of an ELISA and western blotting). The HIV-seropositive patients were significantly older than the HIV-seronegative patients (31.4 +/- 3 years and 24 +/- 1 year, respectively). Two of the seven HIV-seropositive patients presented with severe CD4 lymphocyte depletion. The other five HIV-seropositive patients presented with CD4 lymphocyte counts of 473 +/- 155 (mean +/- SE). Regardless of HIV serological status, all patients demonstrated a severely depressed mitogenic response when compared with control subjects. There were no remarkable differences in complete blood cell counts and differentials within each serological group. Significant differences, however, were noted when CD4/CD8 lymphocyte counts and ratios were measured. Identification of clinical presentations, such as painful gingivitis, that reflect an early stage of HIV infection could aid in the timing of therapy and prevention of the spread of HIV infection.

Adult

Gender-associated differences in rat renal tubular amantadine transport and absence of stereoselective transport inhibition by quinine and quinidine in distal tubules.

The present studies compared male and female rat renal proximal and distal tubular uptake of amantadine, in relation to their transport kinetics and enantioselective inhibition by two diastereoisomers, 8S,9R-(-)-quinine and 8R,9S-(+)-quinidine. Under control conditions, amantadine was concentrated by both tubule fractions with a gender difference for distal tubules (tissue:medium ratio, 18.0 +/- 1.4 for males and 11.0 +/- 0.6 for females; mean +/- S.E.M., P < .05). This was reflected by a higher Km value only in female distal vs. proximal tubular tissue (153 +/- 8 vs. 108 +/- 9 microM; P < .01) but decrease in Vmax values in distal compared to proximal tubules (P < .01) showed no gender-related difference. In proximal tubules, 8S,9R-(-)-quinine and 8R,9S-(+)-quinidine competitively inhibited amantadine transport with apparent inhibitory potency of 2- to 3-fold in favor of 8S,9R-(-)-quinine (P < .01) and without gender preference. Conversely in distal tubules, competitive inhibition of amantadine transport was also elicited by either 8S,9R-(-)-quinine or 8R,9S-(+)-quinidine at a similar concentration range (10-1000 microM), with absence of chiral or gender preference. The present transport data have demonstrated an apparent absence of stereoselectivity in distal tubular uptake inhibition of amantadine, and are suggestive of disparate pathways and/or rate limiting steps involved between renal proximal and distal tubular handling of chiral organic cations for both genders, and between genders for distal tubular transport of amantadine.

Amantadine

Correlation of immunoglobulin and C reactive protein levels in ankylosing spondylitis and rheumatoid arthritis.

Serum C reactive protein (CRP), IgG, and IgA levels were measured in 22 patients with ankylosing spondylitis (AS) and in 20 patients with rheumatoid arthritis (RA) to study the regulation of these proteins in inflammatory disease states. In both RA and AS the mean CRP, IgG, and IgA levels were raised above normal values. Although IgA and CRP levels showed a significant positive correlation in RA (r = 0.53, p = 0.02), there was no correlation between these values in AS (r = 0.24, p = 0.29). The difference in correlation coefficients between the AS and RA groups was significant at a p = 0.05 level. In RA the raised IgA levels may be another manifestation of the acute phase response, as shown by the good correlation between IgA and CRP in that disease. In AS, however, the IgA levels, although raised, do not correlate with CRP levels, suggesting that the mechanism of increase of IgA in the two diseases is different. Gut mediated immune stimulation has been proposed as a cause of raised IgA levels in AS.

Adult

A practical cytopathic effect/dye-uptake interferon assay for routine use in the clinical laboratory.

The clinical value of interferon (IFN) level determinations has been demonstrated, but a practical assay procedure for routine use in the diagnostic laboratory has not been available. The authors examined the susceptibility of five cell lines (WISH, HEp-2, Vero, A549, and WI-26VA4) to vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV), and compared the response of these cells to the inhibitory activity of IFN-alpha and IFN-gamma for the respective viral cytopathic effect (CPE). The WISH-EMCV system was the most sensitive for IFN-alpha, and was approximately as sensitive as the HEp-2-VSV system for IFN-gamma. WISH cells were found to be significantly more sensitive for both IFN-alpha and IFN-gamma when EMCV, instead of VSV, was used (P less than 0.001). Therefore, the latter system served as the basis for developing a CPE dye-uptake procedure that was found to be considerably more rapid but slightly less sensitive than the conventional technic. However, both procedures were equally reproducible and should be suitable for automation.

Amnion

Failure of preexisting antibody against hepatitis B surface antigen to prevent subsequent hepatitis B infection.

We studied a patient who developed acute hepatitis B virus (HBV) infection despite the presence of preexisting antibody to the surface antigen of HBV (anti-HBs). Anti-HBs has been reported to consist primarily of antibody against the common a determinant of HBV. Antibody directed against this major determinant appears to confer protection against HBV, regardless of the subtype. Our patient was shown to have had preexisting anti-HBs of anti-d but not anti-a specificity. She subsequently developed non-A, non-B viral hepatitis followed by an episode of acute hepatitis B after exposure to HBV of the ayw subtype.

Adult

Determination of immunoglobulin M antibodies against hepatitis B core antigen and hepatitis A virus by reorienting sucrose gradient high-speed centrifugation for diagnosis of acute viral-hepatitis.

Immunoglobulin M (IgM) antibodies against hepatitis B core antigen (anti-HBc) and hepatitis A virus (anti-HAV) were determined in 41 cases of acute viral hepatitis. In sera positive for anti-HBc or anti-HAV, IgM was separated from IgG by reorienting sucrose gradient high-speed centrifugation, and the IgG- and IgM-containing serum fractions were tested for the presence of specific antibody by radioimmunoassay. At the onset of illness, 4 of the 41 cases were classified as hepatitis A, 31 were hepatitis B, and 6 were non-A, non-B hepatitis, based on the results of these tests and of assays for hepatitis B surface antigen and antibody and hepatitis B e antigen and antibody. Fourteen of these 41 patients (34%) required IgM anti-HBc or IgM anti-HAV testing or both for appropriate classification. IgM anti-HBc persisted for at least 7 weeks after onset but no longer than 17 weeks in all patients tested with transient hepatitis B surface antigen-positive acute hepatitis. IgM anti-HAV persisted up to but not longer than 62 days in the patients with hepatitis A. Therefore, IgM anti-HBc and IgM anti-HAV determinants are valuable tools for the differential diagnosis of acute A, B, and non-A, non-B hepatitis.

Antibodies, Viral

Hepatitis B virus surface and core antigens in the liver of primary hepatocellular carcinoma cases in Virginia.

Zenker-fixed paraffin-embedded sections of biopsy liver tissue from 64 cases of primary hepatocellular carcinoma (PHC) were stained for hepatitis B surface antigen (HBsAg) and for hepatitis B core antigen (HBcAg) by histochemical and/or immunohistochemical techniques in a retrospective study. PHC arose in livers with postnecrotic cirrhosis in 30 (46.9%) cases. Controls included liver biopsy sections from 123 miscellaneous liver disorders and from 67 randomly selected autopsy specimens, none of which were known to be associated with hepatitis B virus (HBV) infection. HBsAg was detected in tumorous hepatocytes in only one of the 64 cases of PHC. HBsAg was identified in nontumorous hepatocytes of 8 (20%) of 40 specimens that contained adequate nontumorous liver tissue. All of these HBsAg positive cases of PHC were associated with cirrhosis. Thus HBsAg was detected in 8 (33.3%) of 24 cases of PHC with cirrhosis, but in none of the remaining 16 cases without cirrhosis. HBcAg was not detected in the hepatocytes of those HBsAg positive PHC cases tested. Our results suggest that HBV infection may successively lead to chronic hepatitis, cirrhosis and ultimately PHC.

Adolescent

Fatal cytomegalic inclusion disease. Associated skin manifestations in a renal transplant patient.

A case of cytomegalovirus-induced vasculitis led to skin ulcerations in a renal transplant patient. Light and electron microscopy revealed inclusion bodies and viral particles, respectively, characteristic of cytomegalovirus. To our knowledge, this is the first report of cytomegalovirus-induced vasculitis producing skin ulcerations, and it illustrates another of the protean manifestations of cytomegalovirus inclusion disease that may have important clinical implications.

Adult