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L Patel

Publications and source records attributed to L Patel.

87 records · Page 5Linked to original sources

Preparation, characterization, and properties of monoclonal antibodies against the lac carrier protein from Escherichia coli.

Monoclonal antibodies directed against the lac carrier protein purified from the membrane of Escherichia coli were prepared by somatic cell fusion of mouse myeloma cells with splenocytes from an immunized mouse. Several clones produce antibodies that react with the purified protein as demonstrated by solid-phase radioimmunoassay and by immunoblotting experiments; culture supernatants from the clones inhibit active transport of lactose in isolated membrane vesicles. Five stable clones were selected for expansion, formal cloning, and production of ascites fluid, and the antibodies secreted in vivo by each clone also were found to inhibit lactose transport. Antibody from hybridoma 4B1, an IgG2a immunoglobulin, inhibits active transport of lactose in proteoliposomes reconstituted with purified lac carrier and in right-side-out membrane vesicles. In contrast, the antibody has no effect on the generation of the proton electrochemical gradient by membrane vesicles nor does it alter the ability of vesicles containing the lac carrier to bind p-nitrophenyl-alpha-D-galactopyranoside. In order to achieve 50% inhibition of transport activity, a 2- to 3-fold molar excess of antibody to lac carrier is required, regardless of the amount of lac carrier in the membrane. Thus, the concentration of antibody required for a given degree of inhibition is proportional to the amount of lac carrier in the membrane. Finally, antibody-induced inhibition occurs within seconds, an observation suggesting that the epitope is accessible on the surface of the membrane.

Animals↗

Influence of cimetidine on pharmacokinetics of propranolol.

Whole-blood propranolol concentrations were estimated for 12 hours after a single 80 mg oral dose was given in six patients taking cimetidine and two weeks after they had stopped the drug. Mean blood propranolol concentrations were higher throughout the sampling period when the patients were taking cimetidine than when they were not, and the difference was statistically significant between one and four hours (p less than 0.05). The mean relative bioavailability of propranolol, measured as the area under the concentration time curve, was significantly higher when the patients were taking cimetidine (p less than 0.025). The mean increase in bioavailability was 136.5 +/- 57.6%, and the results were consistent in each subject. It is concluded from these results that cimetidine reduces the hepatic first-pass extraction of propranolol.

Adult↗

Mexiletine in human blood and breast milk.

Twelve paired samples of breast milk and blood were obtained, between the 2nd and 5th days after she had given birth, from a 30-year-old woman who was a 8-hourly propranolol (20 mg) and mexiletine (200 mg). Propranolol was detected in 9 of the samples of blood and in only 4 of the milk samples. Mexiletine was measurable in all samples, and the milk : plasma ratio varied between 0.79 and 1.89 with a mean of 1.45. However, the large volume of distribution of mexiletine makes it unlikely that the small dose of the drug received from the milk would be detrimental to the health of infants.

Adult↗

Electrochemical proton gradient in inverted membrane vesicles from Escherichia coli.

Inverted membrane vesicles prepared from Escherichia coli ML 308-225 generate a transmembrane electrochemical proton gradient (delta mu H+; interior positive and acid) during oxidation of D-lactate, succinate, reduced phenazine methosulfate, or NADH or hydrolysis of ATP. Using the distribution of the lipophilic anion thiocyanate to measure the membrane potential (delta psi) and the permeant weak base methylamine to measure the pH gradient (delta pH), maximal values for delta psi H+ of approximately +160 mV are obtained. Many of the properties of delta psi H+ in inverted vesicles are similar to those described previously in right-side-out vesicles [Ramos, S., & Kaback, H.R. (1977) Biochemistry 16, 848]: (1) the magnitude of the delta psi (interior positive) generated in the presence of D-lactate or reduced phenazine methosulfate is similar to that observed in right-side-out vesicles but of opposite polarity and independent of pH from 5.5 to 8.0; (2) plots of delta pH vs. internal pH in the right-side-out vesicles are similar with D-lactate as the electron donor; (3) as observed with right-side-out vesicles, dissipation of delta psi or delta pH leads to a concomitant increase in the other parameter without a change in the rate of respiration; (4) inverted vesicles catalyze Na+ accumulation, and it is apparent that the process can be driven by either delta psi (interior positive) or delta pH (interior acid).

Biological Transport↗

Effect of diethylpyrocarbonate on lactose/proton symport in Escherichia coli membrane vesicles.

Exposure of Escherichia coli ML 308-225 membrane vesicles to the histidine-specific reagent diethylpyrocarbonate (DEPC) led to concentration- and time-dependent inactivation of active lactose transport, and the sensitivity of the system to inactivation was enhanced when an electrochemical proton gradient (delta- muH+, interior negative and alkaline) was generated across the vesicle membrane. Although beta-D-galactopyranosyl 1-thio-beta-D-galactopyranoside blocked DEPC inactivation, binding of p-nitrophenyl alpha-D-galactopyranoside was not significantly altered, indicating that DEPC does not react at the binding sites of the lac carrier protein. Strikingly, vesicles treated with DEPC exhibited an increased apparent Km for delta- muH+-driven lactose transport and counterflow but no change in the Vmax of these reactions and no change in the apparent Km or Vmax of facilitated diffusion. Moreover, DEPC treatment increased the apparent Km observed for delta- muH+-driven proline and D-lactate transport with no change in Vmax. Finally, the lactose counterflow activity of DEPC-treated vesicles was regenerated by subsequent exposure to hydroxylamine. It is suggested that a histidyl residue(s) in the lac carrier or another protein in the translocation complex is involved either in the binding and translocation of protons or in a conformational change that may occur upon protonation of the lac carrier protein.

Biological Transport, Active↗

The role of the carbodiimide-reactive component of the adenosine-5'-triphosphatase complex in the proton permeability of Escherichia coli membrane vesicles.

Membrane vesicles isolated from wild-type and dicyclohexylcarbodiimide-resistant strains of Escherichia coli exhibit identical respiration-dependent transport activities, and in both cases, this activity is abolished by extraction of the vesicles with 1.0 M guanidine-HCl. Transport activity of extracted wild-type vesicles is completely restored by exposing the vesicles to lipophilic or water-soluble carbodiimides, while transport activity of the mutant vesicles is not restored by exposure to lipophilic carbodiimides. Strikingly, however, complete reactivation of transport in mutant vesicles is observed with water-soluble carbodiimides. Similarly, the Ca2+, Mg2+-stimulated ATPase activity of wild-type vesicles is inhibited by both classes of carbodiimides, while the ATPase activity of mutant vesicles is inhibited by water-soluble carbodiimides, but resistant to inhibition by lipophilic carbodiimides. The carbodiimide-reactive component of the membraneous Ca2+, Mg2+-stimulated ATPase complex in wildtype vesicles is readily labeled with N,N'-dicyclohexyl[14C]-carbodiimide, while the analogous component in mutant vesicles is not reactive. Alternatively, when vesicles are treated with 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide [14C]methiodide, a water-soluble carbodiimide, the carbodiimide-reactive component is labeled to a similar degree in both preparations. The results suggest that the altered carbodiimide-reactive proteolipid in the dicyclohexylcarbodiimide-resistant mutant is specifically defective in its ability to react with lipophilic carbodiimides. In addition, these and other findings indicate that the increase in proton permeability observed on extraction of isolated membrane vesicles with chaotropic agents is due exclusively to an effect on the carbodiimide-reactive component of the Ca2+, Mg2+-stimulated ATPase complex.

Adenosine Triphosphatases↗

Absence of an intracellular cobalamin-binding protein in cultured fibroblasts from patients with defective synthesis of 5'-deoxyadenosylcobalamin and methylcobalamin.

Three distinct classes of human mutations (cbl A, cbl B, and cbl C) cause defective synthesis of cobalamin (Cbl; vitamin B(12)) coenzymes. Cultured fibroblasts from that unique class (cbl C) deficient in the synthesis of both Cbl coenzymes, 5'-deoxyadenosylcobalamin (AdoCbl) and methylcobalamin (MeCbl), were used to explore the underlying defect. We compared the uptake of transcobalamin II(TC II)-bound cyano[(57)Co]cobalamin (CN-Cbl) by cbl cells with that of other control and mutant cell lines. Although the cbl C cells initially took up CN-[(57)Co]Cbl normally, they were unable to retain it. To characterize this "leak" further, cell extracts were prepared following incubation and chromatographed on Sephadex G-150. After incubations of 1-2 hr, most of the CN-[(57)Co]Cbl accumulated by control cells was still bound to TC II; the remainder was free. Thereafter, an ever-increasing fraction of the labeled Cbl eluted with an intracellular cobalamin-binding protein (ICB); more than 80% of the total was so bound after 76 hr incubations. ICB had an apparent molecular weight similar to that of several Cbl "R" binders (about 120,000), but was distinguished from them by its failure to react with specific anti-"R"binder antiserum. Significantly, no ICB was detected in extracts of three different cbl C lines even aftr prolonged incubations, whereas its appearance in cbl A, cbl B, and mutase apoenzyme mutants was normal. We propose: that ICB is required for retention of cobalamins by cells; and that cbl C cells "leak" cobalamins and show defective synthesis of Cbl coenzymes because they lack this intracellular binder.

Journal Article↗

Reversible effects of chaotropic agents on the proton permeability of Escherichia coli membrane vesicles.

Extraction of E. coli ML 308-225 membrane vesicles with chaotropic agents causes the vesicles to become specifically permeable to protons. As a result, the vesicles no longer generate a membrane potential, interior negative, and they do not catalyze respiration-dependent lactose or proline transport. Treatment of the extracted vesicles with various carbodiimides decreases the permeability of the vesicle membrane to protons, causing them to regain their ability to generate a membrane potential. By this means, active transport is completely reactivated. Exposure of the vesicles to carbodiimides prior to extraction with chaotropic agents makes transport activity impervious to the effects of the chaotropes.

Biological Transport, Active↗

Gonadotrophin-independent precocious puberty and dyschondrosteosis.

We present a case of gonadotrophin-independent precocious puberty, as seen in McCune-Albright syndrome, and Leri-Weill dyschondrosteosis in a six and a half year-old girl. Her father also reports having early puberty and is similarly affected with dyschondrosteosis. This combination of features has not been reported previously, and represents the association of a skeletal dysplasia with an endocrinopathy.

Bone Diseases, Developmental↗

Serum leptin and leptin binding activity in children and adolescents with hypothalamic dysfunction.

Marked disturbance in eating behaviour and obesity are common sequelae of hypothalamic damage. To investigate whether these were associated with dysfunctional leptin central feedback, we evaluated serum leptin and leptin binding activity in 37 patients (age 3.5-21 yr) with tumour or trauma involving the hypothalamic-pituitary axis compared with 138 healthy children (age 5.0-18.2 yr). Patients were subdivided by BMI <2 SDS or > or = 2 SDS and healthy children and children with simple obesity of comparable age and pubertal status served as controls. Patients had higher BMI (mean 1.9 vs 0.2 SDS; p <0.001), a greater proportion had BMI > or = 2 SDS (54% vs 8%; p <0.001) and higher serum leptin (mean 2.1 vs 0.04 SDS; p <0.001) than healthy children. Serum leptin (mean 1.1 vs -0.1 SDS; p = 0.004) and values adjusted for BMI (median 0.42 vs 0.23 microg/l:kg/m2; p = 0.02) were higher in patients with BMI <2 SDS. However, serum leptin adjusted for BMI was similar in patients with BMI > or = 2 SDS compared to corresponding controls (1.08 vs 0.95; p = 0.6). Log serum leptin correlated with BMI SDS in all subject groups but the relationship in patients with BMI <2 SDS was of higher magnitude (r = 0.65, slope = 0.29, p =0.05 for difference between slopes) than in healthy controls (r = 0.42, slope = 0.19). Serum leptin binding activity (median 7.5 vs 9.3%; p = 0.02) and values adjusted for BMI (median 0.28 vs 0.48 % x m2/kg; p <0.001) were lower in patients than in healthy children. The markedly elevated leptin levels with increasing BMI in non-obese patients with hypothalamic-pituitary damage are suggestive of an unrestrained pattern of leptin secretion. This along with low leptin binding activity and hence higher free leptin levels would be consistent with central leptin insensitivity.

Adipose Tissue↗