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Biomedical subjects

J R Hamilton

Publications and source records attributed to J R Hamilton.

At least 19 recordsLinked to original sources
PubMed1992

Differences in Ca(2+)-mediation of hypotonic and Na(+)-nutrient regulatory volume decrease in suspensions of jejunal enterocytes.

We determined differences in the Ca2+ signalling of K+ and Cl- conductances required for Regulatory Volume Decrease (RVD) in jejunal villus enterocytes passively swollen (0.5 or 0.95.isotonic) compared with swelling because of the absorption of D-glucose (D-Glc) or L-Alanine (L-Ala). Cell volume was measured using electronic cell sizing. In nominally Ca(2+)-free medium containing EGTA (100 microM) RVD after 0.5 or 0.95.isotonic challenge was prevented. L-Ala swelling and subsequent RVD was influenced in Ca(2+)-free medium. Villus cells were incubated with 10 microM of the acetomethoxy derivative of 1,2.bis (2-aminophenoxy) ethane N,N,N1,N1 tetracetic acid (BAPTA-AM) and RVD after 0.5.isotonic swelling or L-Ala swelling was prevented. Niguldipine (0.1 microM), nifedipine (5 microM), diltiazem (100 microM), Ni2+, and Co2+ (1 mM) all prevented hypotonic RVD but had no effect on RVD after L-Ala addition. Charybdotoxin (25 nM) a potent inhibitor of Ca(2+)-activated K+ channels, had no effect on hypotonic RVD but prevented RVD of villus cells swollen by D-Glc. We used the calmodulin antagonists, naphthalene sulfonamide derivatives W-7 and W-13, to assess calmodulin activation of K+ and Cl- conductance in these two models. L-Ala swelling and subsequent RVD was not influenced by 25 microM W-7; hypotonic RVD was prevented by 25 microM W-7 or 100 microM W-13. The W-13 inhibition of RVD was by-passed with 0.5 microM gramicidin. Our data show that hypotonic RVD requires extracellular Ca2+ and that the K+ conductance activated is not charybdotoxin sensitive but requires calmodulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Prevalence of measles antibodies in adults with HIV infection: possible risk factors of measles seronegativity.

OBJECTIVES: To determine the prevalence of measles (rubeola) immunity in a group of HIV-1-infected adults and to examine predictors of measles seronegativity in this population. SETTING: County hospital outpatient clinic and public-health department early HIV intervention clinic. PATIENTS: A total of 262 HIV-infected adults presenting to outpatient clinics between September 1990 and January 1991. INTERVENTIONS: Patients were screened for the presence of measles immunoglobulin G antibody, as measured by an enzyme-linked immunosorbent assay (ELISA). Pertinent clinical and immunologic information was recorded. Univariate and multivariate analyses were performed to identify possible risk factors for measles seronegativity. MAIN OUTCOME MEASURE: Measles seronegativity, as defined by a lack of detectable antibody (ELISA predicted index value < 1.0). RESULTS: Thirteen (5%) patients lacked serologic evidence of immunity. Risk factors for measles seronegativity included year of birth in 1957 or later, Caucasian (non-Hispanic) race and oral hairy leukoplakia. Factors associated with progressive HIV disease (other than hairy leukoplakia) were not associated with a lack of existing immunity. CONCLUSIONS: A high prevalence (95%) of measles antibody was found in this large group of HIV-infected adults. Young, white individuals born in 1957 or later were at the greatest risk for measles seronegativity, but declining immunity due to progressive HIV infection did not appear to be associated with a lack of antibody. Self-reported histories of measles infection or immunization were not reliable predictors of measles immunity.

AIDS-Related Opportunistic Infections↗
PubMed1992

Effect of protein kinase C inhibitors on Cl- conductance required for volume regulation after L-alanine cotransport.

We used electronic cell sizing and Cl- efflux measurements in guinea pig jejunal enterocytes to study activation of Cl- conductance under two experimental conditions, regulatory volume decrease (RVD) after passive hypotonic swelling and volume regulation during Na(+)-alanine cotransport. RVD after a hypotonic (0.5 x isotonic) challenge was not affected by the protein kinase C (PKC) inhibitor 100 microM 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7). Volume decrease after cell swelling in response to L-Ala (25 mM) was prevented by H-7 (P less than 0.05) or the more potent PKC inhibitor 10 nM staurosporine (P less than 0.001). L-Ala stimulated biphasic 36Cl efflux, a rapid efflux over 60 s which was inhibited by H-7 (P less than 0.01) and the Cl(-)-channel blocker anthracene-9-carboxylic acid (9-AC) (P less than 0.005). In contrast, after hypotonic dilution the rate of 36Cl efflux increased (P less than 0.005); H-7 had no effect but 9-AC inhibited the increase (P less than 0.01). Gramicidin (0.5 microM) added to cells maximally swollen by L-Ala in Cl(-)-containing medium caused 2 degree swelling (P less than 0.001), but 10 nM staurosporine reduced this 2 degree swelling (P less than 0.001). Addition of phorbol ester or synthetic diacylglycerol to villus cells under isotonic conditions, after gramicidin addition, caused cell swelling (P less than 0.005) that was inhibited by staurosporine (P less than 0.05). We concluded that PKC does not activate Cl- conductance for hypotonic RVD but that Na(+)-nutrient cotransport is a physiological stimulus for PKC to activate Cl- conductance necessary for volume regulation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Effect of osmotic swelling on K+ conductance in jejunal crypt epithelial cells.

To further elucidate differences in ion transport properties between jejunal crypt and villus cells, we compared the responses of purified cell suspensions to hypotonic stress using electronic cell sizing to evaluate volume changes and 86Rb and 36Cl efflux. After hypotonic swelling, villus enterocytes undergo a regulatory volume decrease (RVD) due to the loss of K+ and Cl- through volume-activated conductances. After 0.6x isotonic challenge in Na(+)-free medium, crypt cells exhibited only partial RVD, with t1/2 congruent to 15 min. The addition of a cation ionophore, gramicidin (0.25 microM), to hypotonically swollen crypt cells caused an accelerated RVD, which was complete with t1/2 congruent to 5 min. Crypt epithelial cells showed no volume-activated 86Rb efflux, but villus enterocytes had an increased rate of 86Rb efflux after hypotonic dilution (P less than 0.001). Gramicidin added to hypotonically diluted crypt cells greatly increased the rate of 86Rb efflux compared with controls. Both villus (30 s; P less than 0.005) and crypt (2 min; P less than 0.001) cells exhibited volume-activated 36Cl efflux in absence of gramicidin. Cl- channel blockers anthracene-9-carboxylate (9-AC, 300 microM) and indanyloxyacetic acid (IAA-94, 100 microM) prevented crypt RVD (P less than 0.001) in the presence of gramicidin. Ouabain (P less than 0.001) or K(+)-free Na(+)-containing medium, but not Ba2+ (5 mM) or quinine (100 microM), prevented crypt partial RVD. We conclude that crypt cells lack volume-activated K+ conductance. The RVD exhibited by crypt cells, although partial, was due to Cl- loss through a volume-activated Cl- conductance and Na+ loss via Na(+)-K(+)-ATPase.

Animals↗
PubMed1991

Corticostatic peptides cause nifedipine-sensitive volume reduction in jejunal villus enterocytes.

We studied cell-volume changes caused by adding corticostatin (CS) or defensin-like peptides to villus enterocytes isolated in suspension from guinea pig jejunum. Guinea pig CS (10(-9) M) added to villus cells in Na(+)-containing medium reduced volume, but immediate cell swelling was caused by 10(-6) M guinea pig CS. In Na(+)-free N-methyl-D-glucamine-containing medium 10(-9) M guinea pig CS accelerated the initial rate of shrinkage compared with cells in N-methyl-D-glucamine-containing medium alone as well as causing greater cell shrinkage. Guinea pig CS-stimulated cell shrinkage was prevented by a Ca2(+)-channel blocker--5 microM nifedipine, by chelation of extracellular Ca2+ with 100 microM EGTA, or by omega-conotoxin (10(-9) M). The Ca2+ ionophore A23187 (2.5 microM) reduced volume when added to villus cells in N-methyl-D-glucamine-containing medium; this action was prevented by EGTA, or quinine--an inhibitor of K+ conductance, or 9-anthracenecarboxylic acid--a Cl- channel blocker, suggesting that the volume reduction occurred because K+ and Cl- conductances were activated. Guinea pig CS-stimulated volume reduction was also prevented by 100 microM quinine or 9-anthracenecarboxylic acid. We conclude that jejunal villus enterocytes possess a Ca2(+)-activated Cl- conductance and a K+ conductance that need not be stretch-activated. Corticostatic peptides cause volume reduction in villus cells by activating L-type Ca2+ channels; other defensin-like peptides were without effect.

Amino Acid Sequence↗
PubMed1991

Alternative technique for repair of sinus venosus atrial septal defect.

A technique is described for closure of a sinus venosus atrial septal defect using a single patch held in place by sutures placed from outside the right atrium and underneath the superior vena cava. The superior vena cava does not require enlargement and potential damage to the artery to the sinoatrial node is avoided.

Adolescent↗
PubMed1991

Performance of cryptococcus antigen latex agglutination kits on serum and cerebrospinal fluid specimens of AIDS patients before and after pronase treatment.

Cryptococcal antigen titers in 97 serum and 42 cerebrospinal fluid (CSF) specimens from 37 AIDS patients with culture-proven cryptococcal infection were determined with the Meridian kit (Meridian Diagnostics Inc., Cincinnati, Ohio) before and after treatment with pronase. The geometric mean titers before and after pronase treatment were 1:45 and 1:588 in serum and 1:97 and 1:79 in CSF, respectively. Only on serum (but not CSF) specimens after pronase treatment were (i) titers increased by 2 to 13 dilutions on 57% of the specimens, all of which had titers of less than or equal to 1:128 before pronase treatment, (ii) false-negative reactions on 27% of specimens before pronase treatment eliminated, all of which had titers from 1:4 to 1:4,096, (iii) prozone-like reactions (titer, less than or equal to 1:256) on 9% of the specimens before pronase treatment eliminated, and (iv) agglutination reactions on all specimens stronger and easier to interpret. Antifungal agents added to serum as well as freeze-thaw cycles did not change antigen titers in serum. After two separate tests, the same titers were obtained on 94% of 35 serum specimens that were treated with pronase and on 96% of 53 CSF specimens that were not treated with pronase. A total of 26 serum specimens and 28 CSF specimens from patients with no cryptococcal disease were negative before and after pronase treatment. The IBL kit (International Biological Labs Inc., Cranbury, N.J.) was compared with the Meridian kit on 41 serum specimens and 14 CSF specimens. Results from the two kits agreed on 54 and 68% of serum specimens and 86 and 93% of CSF specimens before and after pronase treatment, respectively. The IBL kit generally produced higher titers on specimens in disagreement and produced no prozone-like reactions. Routine pronase treatment of serum is recommended with the Meridian kit in order to eliminate false-negative and unclear agglutination reactions by producing a consistent interpretation of agglutination reactions. CSF specimens do not require pronase treatment. Titer results produced by the kits from the two different manufacturers varied considerably: the kits should not be used interchangeably for determining antigen titers in serum specimens.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Volume regulation initiated by Na(+)-nutrient cotransport in isolated mammalian villus enterocytes.

We assessed ion transport during regulatory volume decrease (RVD) in jejunal villus enterocytes, isolated in suspension from guinea pig jejunum and swollen by exposure to L-alanine (L-Ala) or D-glucose (D-Glc) in the presence of Na+. Cell volume was measured electronically. Relative volume of cells (rel vol: cell vol/isotonic vol) within 1 min of L-Ala (20 mM) addition increased (1.10 +/- 0.03, P less than 0.005), but by 5 min there was no difference between cells in L-Ala or 20 mM D-Ala (0.95 +/- 0.02). Cell shrinkage after maximal swelling was greater with L-Ala than with D-Ala (14 +/- 4 vs. 2 +/- 1%, P less than 0.01). Initial swelling generated by L-Ala required extracellular Na+ (P less than 0.02). Volume increased 30 s after D-Glc (20 mM), and cells were larger than cells treated with L-Glc (1.04 +/- 0.01 vs. 0.95 +/- 0.01, P less than 0.001); subsequent cell shrinkage was complete in 2 min (8 +/- 2%, P less than 0.05). Swelling generated by methyl alpha-D-glucoside was prevented by 0.1 mM phloridzin (P less than 0.05). RVD after D-Glc swelling was prevented by inhibitors of K+ channels, 5 mM Ba2+ (P less than 0.001), 100 microM quinine (P less than 0.005), or 25 mM TEA (P less than 0.02), but the same inhibitors completely prevented L-Ala swelling. All inhibitors had no effect on L-Ala uptake into brush-border membrane vesicles in presence of Na+ gradient.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
PubMed1991

Separate K+ and Cl- transport pathways are activated for regulatory volume decrease in jejunal villus cells.

We assessed ion transport mechanisms operative during regulatory volume decrease (RVD) in jejunal villus enterocytes, isolated in suspension from guinea pig jejunum and examined with electronic cell sizing. Immediately after reduction of osmolarity (153 mosmol/kg medium) enterocytes swelled, but within 5 min they shrank by 50%. This RVD, which was complete by 20 min, was unaffected by Li+ substitution for Na+ or by Na(+)-free (N-methyl-D-glucose, NMDG+) medium. Passive loss of K+ is required for RVD because both the magnitude and direction of RVD changed when external [K+] varied. Increasing K+ permeability with gramicidin (0.5 microM) accelerated RVD in NMDG+ medium (10.0 +/- 0.8 vs. 6.2 +/- 0.4% min-1, P less than 0.01) suggesting that K+ loss is rate limiting for RVD. Inhibition of K(+)- and Ca2(+)-activated K+ conductance with Ba2+ (5 mM, P less than 0.005), quinine (100 microM, P less than 0.005), or apamin (1 microM, P less than 0.005) prevented RVD. Inhibition of Cl- conductance with 9-anthracenecarboxylic acid (100 microM, P less than 0.005) or dipyridamole (75 microM, P less than 0.005) also prevented RVD. In isotonic HCO3(-)-buffered medium, the addition of gramicidin to cells generated conditions in which anion permeability was rate limiting for cell swelling. This swelling was inhibited 97% by 100 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). In K(+)-free, HCO3(-)-buffered medium containing DIDS and gramicidin hypotonic swelling resulted in continued (secondary) swelling (rel vol 1.19 +/- 0.01 vs. 1.25 +/- 0.02, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Paralysed diaphragm after cardiac surgery in children: value of plication.

Over a 2-year period (1987-1988), 31 children (3% of 960 operations) were found to have a paralysed diaphragm following cardiac surgery. The median age was 5 months with 65% less than 1 year of age. In the 31 patients, 38 paralysed diaphragms were identified. The phrenic nerve injury was on the right in 8 cases, the left in 16, bilateral in 7 and 40% were related to modified Blalock Taussig shunts. The time to extubation was analysed for each patient in two separate groups: Group A: (greater than 1 year): 11 children of whom 5 were extubated without difficulty, 4 had non-respiratory reasons for prolonged ventilation and only 2 were plicated--both were extubated within 4 days. Group B: (less than 1 year): 20 infants of whom 16 were plicated and 4 were not. Three of the children who were plicated died from cardiac causes. Of the 13 survivors, there were 3 who had other reasons for prolonged ventilation. Thus 10 infants required prolonged ventilation (mean 11 days) because of respiratory difficulties. All underwent plication and were extubated at a mean of 2.4 days postoperatively. The 4 who were not plicated were extubated at a mean of 11 days postoperatively. In infants in whom there is no cardiac cause for failure to wean from ventilation, diaphragmatic paralysis should be suspected and plication performed if not extubated 2 weeks after operation.

Anastomosis, Surgical↗
PubMed1990

Efficacy of short courses of oral novobiocin-rifampin in eradicating carrier state of methicillin-resistant Staphylococcus aureus and in vitro killing studies of clinical isolates.

Methicillin-resistant Staphylococcus aureus (MRSA) is an important nosocomial infection problem. Colonization appears to be more common than invasive disease is. Eradication of colonization or the carrier state could limit the spread of MRSA, thus reducing the potential for mortality and morbidity in other patients. The detection of patients with MRSA infection in a rehabilitation ward led to a study of the combination of novobiocin-rifampin in vivo and in vitro. We found that 300 mg of rifampin plus 500 mg of novobiocin orally twice daily for 5 days, in 18 courses of treatment given to 12 patients, resulted in the clearing of MRSA in 79% of the evaluable courses and 81% of the evaluable sites. A second course cleared MRSA from one of the patients with a treatment failure. Side effects were not noted. All 18 pretherapy isolates were susceptible to either drug in vitro, but 1 of 2 posttherapy isolates was rifampin resistant. Timed-kill studies demonstrated that the rate of killing was the same with either drug alone or both drugs together. Pretherapy isolates from treatment successes or failure were killed at the same rate by the drug combination. However, with the rifampin-resistant isolate killing ceased after 48 h. Results of this study suggest that previously untreated patients are likely to have isolates that are susceptible to the combination of drugs and that the combination is commonly effective in eradicating MRSA carriage. Since the regimen is orally administered, and thus convenient, in conjunction with other measures it has the promise of reducing the spread of MRSA in hospitals.

Administration, Oral↗
PubMed1990

Comparison of Guizotia abyssinica seed extract (birdseed) agar with conventional media for selective identification of Cryptococcus neoformans in patients with acquired immunodeficiency syndrome.

Growth of Cryptococcus neoformans from the sputum of patients with acquired immunodeficiency syndrome may be obscured by oral contamination with Candida albicans on conventional media. We prospectively compared direct plating of sputum and urine onto birdseed agar and compared birdseed agar plating with plating onto Mycosel and Sabouraud dextrose agar cultures. Thirty-two sputum and three urine specimens were compared. C. neoformans was isolated from five specimens. In two specimens, one of sputum and one of urine, C. neoformans was detected only on the birdseed agar plate because of overgrowth on the conventional media by C. albicans. C. neoformans produced dark colonies on birdseed agar, unlike C. albicans, which produces white colonies. The use of birdseed agar as the primary culture medium for sputum and urine specimens from patients with acquired immunodeficiency syndrome increases sensitivity for C. neoformans.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Regulatory volume increase in mammalian jejunal villus cells is due to bumetanide-sensitive NaKCl2 cotransport.

We assessed ion transport mechanisms operative during regulatory volume increase (RVI) in villus enterocytes isolated in suspension from guinea pig jejunum and examined with electronic cell sizing and 86Rb influx. After validation of the electronic-sizing technique with direct measurements of cell water, the response of cell volume to hypertonic media was evaluated in detail. When shrunk by exposure to hyperosmotic media (455 mosmol/kg medium) cells demonstrated a RVI that was complete in 20 min. RVI required extracellular Na+, K+, and Cl-; this cell swelling showed the following ion sensitivity; Na+ greater than Li+ greater than choline, K+ = Rb+, and Cl- greater than or equal to Br- greater than NO3- = acetate = gluconate. Bumetanide inhibition of villus cell swelling was concentration dependent from 10(-10) to 10(-5) M (7.0 +/- 4.5% vs. 87.8 +/- 0.3%); furosemide (10(-3)M) inhibited RVI (74.1 +/- 9.5%), but amiloride (10(-4) M) had little effect on cell swelling. Disulfonic stilbenes, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (10(-4) M), generated the same inhibition of RVI in either nominally HCO3(-)-free phosphate-buffered saline (PBS) or HCO3(-)-buffered PBS, suggesting anion exchange was not involved. Ouabain (10(-4) M) stimulated cell swelling. Hypertonic shrinkage increased the initial rate of bumetanide-sensitive 86Rb influx (80 +/- 38 vs. 1,011 +/- 241 pmol.mg protein-1.min-1; P less than 0.005) and required extracellular Na+ and Cl- (11 +/- 16 vs. 28 +/- 61 pmol.mg protein-1.min-1). RVI was prevented in low-K+ media (0.2 mM), but the addition of KCl initiated cell swelling. Our data strongly suggest that RVI in jejunal villus enterocytes occurs because of the hypertonic activation of NaKCl2 cotransport.

Animals↗
PubMed1979

A clinical study of young infants after small intestinal resection.

We prospectively studied 15 infants who, before 3 months of age, underwent resection of the small intestine-proximal in 3 infants, mid in 6, and distal in 6. Two died before one year of age. Many required prolonged parenteral nutrition, but by one year, 12 of the 13 survivors were on oral feedings only, and seven were above the third percentile for height and weight. Developmental delay occurred in the early postoperative period but diminished with time. There was compensatory adaptation of the remaining gut, shown by improving fat and B12 absorption and duodenal bile-salt concentrations. Bacterial contamination complicating end-to-side anastomoses occurred in two cases (P), gastric hyperacidity in four of 12 (1P, 3M), and hyperoxaluria in eight of 14 (1P, 5M, 2D). Studies of immune competence revealed normal cellular immune function (11/11), transient hypogammaglobulinemia (3/14), hypocomplementemia (1/12), and serum autoantibodies (3/10). Thus, massive resection of the small intestine did not preclude spontaneous improvement in absorptive function, growth, and development.

Child Development↗