Tropheryma whippelii DNA is rare in the intestinal mucosa of patients without other evidence of Whipple disease.

BACKGROUND: Little is known about the pathogenesis of Whipple disease, the reservoirs of Tropheryma whippelii, and the proportion of persons harboring the bacterium without "classic" intestinal abnormalities. OBJECTIVE: To assess the presence of T. whippelii in patients undergoing upper endoscopy for a variety of indications. DESIGN: Prospective and routine diagnostic examination of patients. SETTING: Three academic medical centers in California; Minnesota; and Heidelberg, Germany. PATIENTS: 342 patients undergoing endoscopy for evaluation of dyspepsia or possible peptic ulcer (group A, 173 patients), malabsorption (group B, 37 patients), or clinical suspicion of Whipple disease (group C, 132 patients). MEASUREMENTS: Small-intestinal biopsy specimens were tested by polymerase chain reaction for T. whippelii DNA and examined for histopathologic abnormalities. RESULTS: All patients with negative histologic findings also had negative results for T. whippelii DNA. CONCLUSIONS: T. whippelii occurs only rarely in intestinal mucosa that lacks histopathologic evidence of Whipple disease. The human small intestinal mucosa is an unlikely reservoir for this organism.

A comprehensive breast and cervical cancer screening program for medically underserved women in Connecticut.

A comprehensive breast and cervical cancer early detection program supported by federal and state funds and administered by the Connecticut Department of Public Health, is actively recruiting and screening older, uninsured, low income women at contracted health-care facilities throughout the state. The program provides diagnostic testing, treatment referral, outreach, and educational activities. During the first 27 months of the program, 5,509 women were enrolled and screened. Women were recruited primarily through media sources and physician/nurse referrals. The majority of women served were non-Hispanic white, between ages 40 to 59, with annual incomes of less than $10,000, and a high school education or less. Some 62% of enrolled women either never had a mammogram or did not have a repeat mammogram within the time-frames recommended by ACS. Recruitment efforts continue to enroll medically underserved women for breast and cervical cancer screening services. Future efforts will focus on rescreening in order to achieve the program's overall mission of detecting breast and cervical cancers at earlier stages.

Intra- and submembrane particle densities during CO2 stimulation of H+ secretion in turtle bladder.

The apical cell membranes of the H+ secreting, alpha-intercalated cells of turtle urinary bladder (TB) are characterized by studs (cytoplasmic domains of V-adenosinetriphosphatase) on thin-section transmission electron microscopy and by intramembrane particles (spherical units, SPUs) occurring as rod-shaped particles on freeze-fracture electron microscopy. To examine the relationship between studs and SPUs, morphometric studies were carried out on bladders maintained in 5% CO2 and in the absence of exogenous CO2. The stud density per square micrometer of apical membrane was 3,909 +/- 352 (+/-SE) in four TBs (29 alpha-cells) at 5% CO2 and 3,667 +/- 448 (+/-SE) in the paired halves of the same bladders without CO2 (25 alpha-cells). Corresponding densities of SPUs counted on apical membranes of the same bladders (n = 4) were 3,941 +/- 545 in 5% CO2 and 3,599 +/- 511 without CO2. The similarity of the densities of studs and SPUs under both conditions indicates that each SPU within the membrane is matched by one stud projecting into the cytoplasm. The one-for-one relationship between studs and SPUs was preserved over a wide range of transport rates. Addition of CO2 caused only inconsistent increments in the densities of studs and SPUs despite substantial increases in H+ transport rate. Slight variations in spacing of studs were consistent with patterns of distribution of SPUs on fracture surfaces.

Sch-28080 inhibits bafilomycin-sensitive H+ secretion in turtle bladder independently of luminal [K+].

To explore the possible contribution of an H-K-adenosine-triphosphatase (H-K-ATPase) to H+ secretion (JH) in the isolated turtle bladder, we measured electrogenic JH (JeH) as short-circuit current and total JH (JTH) by pH stat titration in the presence of ouabain at different ambient K+ concentration ([K+]) and during luminal addition of a known gastric H-K-ATPase inhibitor, Schering (Sch)-28080. JH was not reduced by decreasing ambient [K+] to undetectable or very low levels (< 0.05 mM by atomic absorption) and luminal BaCl2 addition to further reduce local [K+] at the apical membrane. These K(+)-removal studies indicate that H+ transport is not coupled to countertransport of K+. JTH did not exceed JeH at any point: in K(+)-free solutions JTH was 0.73 +/- 0.05, and JeH was 0.95 +/- 0.08 mumol/h; in standard (3.5 mM) K+ solutions JTH was 0.72 +/- 0.05 and JeH 0.98 +/- 0.06 mumol/h; in high (118 mM) K+ solutions JTH was 0.65 +/- 0.07 and JeH 0.94 +/- 0.08 mumol/h. Sch-28080 caused a rapid inhibition of JH, with similar half-maximal inhibitory concentrations (IC50) in K(+)-free, standard [K+], and high [K+] solutions. Bafilomycin inhibited JeH and JTH with an IC50 of approximately 100 nM. The observed non-potassium-competitive inhibition of JH by Sch-28080 and the bafilomycin sensitivity distinguish the H-ATPase of the turtle bladder from the gastric H-K-ATPase. The rapidity of the inhibition by Sch-28080 suggests that it acts at an accessible luminal site of the ATPase.

Erotomania in an adolescent: clinical and theoretical considerations.

Erotomania is a relatively rare delusional syndrome, typically seen in heterosexual women of middle-age or beyond. This is the first reported occurrence in an adolescent, and one of very few involving homosexual orientation. A detailed case report is discussed in the context of adolescent developmental phenomena, including "crushes", identity formation, and the resolution of sexual orientation. The presentation of erotomania as alleged sexual abuse, and a possible etiologic role for childhood sexual trauma, are considered.

Characteristics of apical Cl-HCO3 exchanger of bicarbonate-secreting cells in turtle bladder.

The apical anion exchanger of the beta-carbonic anhydrase (CA) cells differs from the basolateral exchanger of the alpha-cells by reduced sensitivity to disulfonic stilbenes and lack of immunoreactivity with antibodies to erythrocyte band 3 protein. To characterize the exchanger, we examined the effects on electroneutral bicarbonate secretion (JHCO3n) of Cl- replacement by gluconate, Br-, SO4(2-), and NO3- and of inhibition by 1) acetazolamide (ACZ) with and without pretreatment with sodium azide (NaN3), 2) furosemide, and 3) alpha-cyano-4-hydroxycinnamate (CHC). The Cl-dependent JHCO3n was 0.90 +/- 0.09 mumol/h, similar to the ACZ-inhibitable rate of 0.83 +/- 0.08 mumol/h with an apparent Km for Cl near 3.4 mM. Maximal JHCO3n was comparable at luminal pH 6.8 and 4.5. JHCO3n was reduced to approximately 21% in Br-, 13% in SO4(2-), and 7% in NO3- solutions compared with the rates in chloride solutions. ACZ inhibition was not abolished by pretreatment with NaN3. JHCO3n was only slightly inhibited (14%) by furosemide and not inhibited by CHC. In conclusion, the apical exchanger is selective for chloride and relatively resistant to inhibitors. Its dependence on luminal chloride is such that its transport rate is closely regulated by mucosal chloride at concentrations below 20 mM.

NBD-taurine uptake by alpha-type carbonic anhydrase cells of turtle bladder.

The uptake of the fluorescent anion, N-(7-nitrobenz-2-oxa-1,3 diazol-4-yl)aminoethanosulfonic acid-taurine (NBD-T) was examined in sheets of turtle bladder epithelial cells after either serosal or mucosal exposure to the fluorescent anion. Serosal uptake of NBD-T into a population of epithelial cells was demonstrated in thin epithelial sheets scraped from bladder sacs exposed to low (0.5 mM) concentrations of NBD-T sufficient to cause fluorescence in turtle erythrocytes. In nine sheets NBD-T fluorescence was observed in 14.4 +/- 1.3% of epithelial cells; by phase-contrast microscopy of the same fields, these cells were nongranular or carbonic anhydrase (CA) cells. An additional 8.1 +/- 1.0% of cells was nongranular, but failed to exhibit fluorescence after serosal NBD-T exposure, consistent with a beta-CA cell population. Apical uptake of NBD-T into epithelial cells was demonstrable only at high (5 mM) mucosal concentrations in both thin sheets and superfused bladder segments. In thin sheets, NBD-T fluorescence was observed in 15.8 +/- 0.7% of cells and appeared to have a punctate subapical distribution; phase-contrast of the same fields (n = 46) revealed a nongranular cell population of 21.9 +/- 0.9%. Nongranular cells corresponded closely to CA cells as identified with carboxyfluorescein fluorescence. Hence, apical NBD-T was taken up primarily by alpha-CA cells. In conclusion, NBD-T is transported by alpha-CA cells either across the basolateral membrane with high affinity comparable to that of turtle red cell band 3 protein or across the apical membrane with low affinity via a less-specific mechanism such as endocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)

A double-membrane model for urinary bicarbonate secretion.

To define the transport pathway for HCO-3 secretion (JHCO3) across the apical and basolateral membranes of turtle bladder, we examined the effects of cAMP, isobutylmethylxanthine (IBMX), the Cl- channel blocker 9-anthroic acid (9-AA), and the disulfonic stilbene DIDS (4,4'-diisothiocyanostilbene-2,2'-sulfonic acid) on the electroneutral and electrogenic components of JHCO3. Total JHCO3 was measured by pH stat titration of the mucosal compartment after Na+ absorption and H+ secretion were abolished by ouabain and a delta pH, respectively. Addition of cAMP or IBMX increased total JHCO3 and induced a short-circuit current (ISC), accounting for a large part of JHCO3; net Cl- absorption was reduced. Mucosal 9-AA inhibited the IBMX-induced electrogenic component of JHCO3, whereas mucosal DIDS inhibited the electroneutral component and acetazolamide reduced both. We suggest that HCO-3 is generated within the cell by a Na-independent primary active acid-base transport at the basolateral membrane (H+ extrusion into the serosal compartment). Cellular HCO-3 accumulation drives JHCO3 via a Cl-HCO3 exchanger at the luminal membrane. IBMX and cAMP activate a 9-AA-sensitive anion conductance parallel to the exchanger. The apparent reversal of the transport elements between the two cell membranes (compared with H+-secreting cells) led to an ultrastructural examination of the carbonic anhydrase-rich cells.

Erythrocyte membrane transport in hypertensive humans and rats. Effect of sodium depletion and excess.

Sodium transport by erythrocyte membranes was studied in hypertensive and normotensive humans and in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). The rate constants of sodium efflux were increased in both hypertensive humans and rats, and this increase was due mostly to an increase in the ouabain-resistant component of efflux. Both the furosemide-sensitive and furosemide-resistant components of efflux were increased. The ouabain-sensitive efflux was also increased, as confirmed by the ouabain-sensitive rubidium influx in rats. In rats, the intracellular sodium content was also increased in the SHR with respect to the WKY. The transport abnormalities of red cell membrane associated with hypertension were similar in humans and rats. In rats, sodium depletion failed to affect the transport abnormality, while sodium load made the difference in transport between SHR and WKY undetectable. Cross-incubation experiments, using plasma and erythrocytes of WKY and SHR, are more suggestive of a flux abnormality that is intrinsic to the cell membrane than of one that is humoral in nature.