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PubMed2005

The prevention of neuroma formation by diathermy: an experimental study in the rat common peroneal nerve.

INTRODUCTION: There have been anecdotal reports of the efficacy of diathermy (electrocoagulation) in the prevention of neuroma formation. However, this has not been investigated in the laboratory. In this experiment involving 40 rats, diathermy was applied to the terminal proximal ends of transected rat common peroneal nerves to evaluate its effect on neuroma formation. MATERIALS AND METHODS: Monopolar and bipolar diathermy set at 45 W, applied for different durations (4 seconds and 10 seconds), were evaluated. Under histological control, the presence of neuroma formation and the diameter of the nerve ends were evaluated at 3 months. The contralateral common peroneal nerve in the same rat served as the control. The dorsal root ganglia of 2 rats in each group were also harvested for histological study. RESULTS: The incidence of neuroma formation was 30% in the group which received high-duration monopolar diathermy (10-second application), versus 90% in the control group (P <0.05). The mean diameter of the nerve ends was smaller at 0.51 mm [standard deviation (SD), 0.29] versus 0.85 mm (SD, 0.24) in the control (P <0.05). The incidence of neuroma formation was 30% in the group which received low-duration monopolar diathermy (4-second application), and 83% in the control group (P <0.05). The diameter was 0.43 mm (SD, 0.14) versus 0.85 mm (SD, 0.28) (P <0.05). High-duration bipolar diathermy applied for 10 seconds, showed a neuroma formation of 25% versus 100% in the control group (P <0.05). The diameter of the nerve ends was 0.48 mm (SD, 0.07) versus 0.79 mm (SD, 0.36) in the control group (P <0.05). The incidence of neuroma formation was 60% in the low-duration bipolar group, which received bipolar diathermy application for 4 seconds, and 90% in the control group (P = 0.25). The diameter of the nerve ends in the low-duration bipolar group was 0.52 mm (SD, 0.24) versus 0.76 mm (SD, 0.40). The incidence of neuroma formation and the difference in diameter in the low duration-bipolar group were both not statistically significant. CONCLUSION: This study demonstrates the effectiveness of monopolar diathermy in reducing the rate of neuroma formation. For bipolar diathermy, an application of 10 seconds was effective in reducing neuroma formation but an application of 4 seconds was not associated with a significant reduction in neuroma formation.

Animals↗
PubMedDate not supplied

[Endogenous colony formation in mice with experimental pathology of the central nervous system].

Models of endo- and exogenous clone formation were used to study colony formation in (CBA X C57B1)F1 mice in different periods after damage to the hypothalamic structures. The following dynamics of colony formation was revealed in the animals with hypothalamic damage in endogenous clone formation: intensified colony formation occurring 24 hours after injury to the brain structures was replaced by a tendency to decrease in 4 days, which was followed by marked inhibition of colony formation 8 days after injury to the hypothalamic structures. The effect of inhibition of colony formation was encountered in animals with damage to the posterior hypothalamic field. No essential changes were revealed in colony formation 4 and 8 hours after hypothalamic injury in exogenous clone formation. Comparison of the results of endo- and exogenous clone formation suggests that the inhibition of colony formation in late-term periods after injury to the posterior hypothalamic field may be due to inhibition of the migration of hematopoietic stem cells from the bone marrow.

Animals↗
PubMed1988

Efficiency analysis of two written short-answer student evaluation formats.

The purpose of this study was to compare the efficiency of two written short-answer student evaluation formats. Efficiency was defined in this study as reliability per unit of examination time. Twenty second-year physical therapy students enrolled in the soft tissue injuries portion of the orthopedic course completed a 12-item quiz consisting of two formats (diagnosis and response set) with six parallel content items per format. The outcome measures of interest were 1) students' score, 2) amount of time required to complete each item, and 3) amount of time required by the faculty members to grade each item. The results indicated that a greater reliability per unit of examination time was achieved for the diagnosis format than for the response set format and that the diagnosis format could be graded more rapidly and with a higher level of interrater agreement than the response set format. Students' grades on the diagnosis format items tended to be higher (although not statistically significant) than the grades on the response set format items, suggesting that when a criterion-referenced system is used, the minimal acceptable baseline score should be raised when using the diagnosis format. Further study is required to evaluate the validity of the diagnosis format.

Educational Measurement↗
PubMed1985

Inhibition of the formation of 5-hydroxy-6,8,11,14-eicosatetraenoic acid from arachidonic acid in polymorphonuclear leukocytes by various coumarins.

The effects of various coumarins (i.e. esculetin, daphnetin and fraxetin) on the formation of the 5-lipoxygenase product, 5-HETE, and the cyclooxygenase product, HHT, were studied. Esculetin (6,7-dihydroxycoumarin) was found to inhibit the formation of 5-HETE more strongly than HHT; its concentrations for 50% inhibition (IC50) were 1.46 +/- 1.02 microM for the formation 5-HETE and 57.3 +/- 17.3 microM for the formation of HHT. Daphnetin (7,8-dihydroxycoumarin) and fraxetin (6-methoxy-7,8-dihydroxycoumarin) also inhibited the formation of the 5-lipoxygenase product, 5-HETE, and the cyclooxygenase product, HHT; their IC50 values were, respectively, 6.90 +/- 2.07 microM and 2.57 +/- 0.088 microM for the formation of 5-HETE and 139.0 +/- 30.0 microM and 532.5 +/- 33.0 microM for the formation of HHT. The monohydroxy coumarin derivatives umbelliferone (7-hydroxycoumarin) and scopoletin (6-methoxy-7-hydroxycoumarin) and the coumarin glucosides fraxin (6-methoxy-7,8-dihydroxycoumarin 8-O-D-glucoside) and esculin (6,7-dihydroxycoumarin 6-O-D-glucoside) also inhibited the formation of 5-HETE, though less strongly. 4-Hydroxycoumarin and coumarin had no effect on either 5-lipoxygenase or cyclooxygenase at concentrations of up to 1 mM. Esculetin inhibited the formation of 5-HETE noncompetitively. In contrast, the dimethoxycoumarin fraxidin (6,8-dimethoxy-7-hydroxycoumarin) inhibited the formation of HHT more strongly than the formation of 5-HETE at a concentration of 1 mM.

Animals↗
PubMed1995

The effect of heterotopic bone formation on prosthetic loosening after total hip replacement.

Seven hundred thirty-two total hip replacements performed from 1970 to 1980 were evaluated for the degree of heterotopic bone formation postoperatively and its effect on long-term mechanical loosening. There were 231 Charnley total hip replacements, of which 152 had no heterotopic bone formation, 58 had Grade 1 formation, and 21 had Grade 2 or 3 formation. Among the 123 Mueller total hip replacements, 98 had no heterotopic bone formation, 19 had Grade 1 formation, and 6 had Grade 2 or 3 formation. For the 378 T-28 total hip replacements, there were 305 with no heterotopic bone formation, 59 with Grade 1 formation, and 14 with Grade 2 or 3 formation. Survival analyses using the definition of failure as loosening, fracture, or revision of the acetabulum or femoral components were constructed. There was no correlation between mechanical loosening, fracture, or revision of the total hip replacement and any degree of heterotopic bone formation.

Arthritis, Rheumatoid↗
PubMed1994

Bioactivation of arachidonic acid by the cytochrome P450 monooxygenases of guinea pig lung: the orthologue of cytochrome P450 2B4 is solely responsible for formation of epoxyeicosatrienoic acids.

Guinea pig lung microsomes converted arachidonic acid (AA) to two classes of cytochrome P450 (P450)-dependent metabolites, 16- through 20-hydroxyeicosatetraenoic acids [(16-20)-OH-AA] and epoxyeicosatrienoic acids (EETs). The rate of formation of (16-20)-OH-AA was approximately 3-fold higher in microsomes from beta-naphthoflavone-induced versus untreated animals. In microsomes from untreated or induced animals EETs, the major class of P450 metabolites in guinea pig lung, were formed in a regioselective manner, with 8,9-, 11,12-, and 14,15-regioisomers accounting for > or = 90% of the total EETs. With isozyme-selective inhibitors and inhibitory antibodies the role of individual pulmonary P450 isozymes in AA metabolism was examined. Metyrapone and SKF-525A (P450 2B selective) inhibited EET formation by > or = 85% with little effect on (16-20)-OH-AA formation. 1-Aminobenzotriazole (1 mM), a mechanism-based inhibitor with low isozyme selectivity, inhibited the formation of both classes of metabolites by > 95%, whereas N-alpha-methylbenzyl-1-aminobenzotriazole (1 microM), a P450 2B-selective mechanism-based inhibitor, abolished EET formation with little effect on (16-20)-OH-AA formation. Antibodies to rabbit P450 2B4 also abolished EET formation without inhibiting the formation of (16-20)-OH-AA, whereas antibodies to rabbit P450 4B1 did not inhibit the formation of either class of metabolites. alpha-Naphthoflavone (P450 1A1 selective in lung) did not inhibit the formation of either class of metabolites. These data demonstrate that the guinea pig orthologue of P450 2B4 is solely responsible for the bioactivation of AA to EETs in guinea pig lung and that a form of P450 other than a 2B, 4B, or 1A isozyme, which is inducible by beta-naphthoflavone, is responsible for (16-20)-OH-AA formation.

8,11,14-Eicosatrienoic Acid↗
PubMed1987

Inhibition of hydroxyl radical formation by human tears.

The effect of human tears on oxygen radical formation was investigated using xanthine-xanthine oxidase as the oxygen radical generating system. Superoxide (O2.-) and hydrogen peroxide (H2O2) were measured using ferricytochrome c as indicator. OH. formation was monitored by measuring the hydroxylation of salicylate. Addition of traces of iron (Fe3+) and chelator (EDTA) was a prerequisite for OH. formation in this system. Human tears did not detectably affect O2.- or H2O2 formation but markedly inhibited OH. formation. Tears obtained from eight different individuals all showed a marked inhibitory effect on OH. formation, whereby only a small individual variation was observed. During separation of human tears by gelfiltration on a Sephadex G75 column, three protein peaks eluted from the column. The first contained lactoferrin, the second as yet unidentified material, and the third lysozyme. Inhibitory activity on OH. formation coincided with the first protein peak and also with fractions eluting after the protein peak containing lysozyme. The major inhibition on OH. formation was seen in these latter fractions, which contain small organic and anorganic substances. The fact that ascorbic acid could not be detected in human tears and that it did not affect formation of OH. in this investigation's assay system indicates that this compound was not involved in the observed low molecular weight inhibitory effect. Analysis of various cations suggested that the low molecular weight inhibitory effect could largely be ascribed to tear calcium. Tear calcium binds to EDTA and thus possibly prevents formation of the essential catalytic iron-EDTA complex. Experiments using purified human milk lactoferrin showed, that this protein, which is abundantly present in human tears, can inhibit OH. formation in the model used here. The inhibitory effect of lactoferrin was counteracted by increasing the iron concentration in the reaction mixtures. These findings suggest that tear lactoferrin may play an important role in the protection of the ocular surface against OH. induced damage.

Eye Proteins↗
PubMed1997

Language arts achievement level, attitude survey format, and adolescents' attitudes towards reading.

The joint effects of student achievement level and attitude survey format upon attitudes toward reading were investigated. Sixth-grade students completed reading attitude surveys involving a standard Likert-type format or one involving pictures of the comic strip character, Garfield. The survey items were identical for both formats; only the presentation format was varied. There was no significant main effect on attitude responses due to achievement level, but the main effect due to survey format was significant, with the Likert-type format producing significantly higher attitude responses than the Garfield format. The interaction between achievement level and format also was significant, with above average students and average students giving higher attitude responses than did below average students when the Garfield format was used. When the Likert-type format was used, average students and below average students gave higher attitude responses than did above average students. The results imply that attitude responses of adolescents can be manipulated by varying the format of the survey.

Achievement↗
PubMedDate not supplied

An enzymatic method for the analysis of formate in human plasma.

An enzymatic method for the determination of plasma formate concentration is described. Formate dehydrogenase is used to reduce NAD+ to NADH in the presence of formate. The resulting NADH then reduces the dye resazurin to resorufin, a reaction catalyzed by the endogenous diaphorase of the plasma. The generated resorufin is then measured fluorimetrically by exciting it at 565 nm and quantitating the emitted light at 590 nm. The method uses the patient's plasma as the blank and as the matrix for the construction of a patient-specific formate calibration curve. The blank contains all components of the assay system except the formate dehydrogenase. Formate concentration is determined from the calibration curve, constructed by adding known quantities of sodium formate to the plasma base, and plotting the fluorescence intensity against formate concentration. The assay which is sensitive to a formate level of 7 mg/L should find application in cases where formate is a metabolite.

Aldehyde Oxidoreductases↗
PubMed2005

Effects of formate on fermentative hydrogen production by Enterobacter aerogenes.

This paper describes the effects of formate on fermentative hydrogen production by Enterobacter aerogenes by way of batch culture. When 20 mM formate was added to pH 6.3 and pH 5.8 E. aerogenes glucose cultures (formate culture) at the beginning of cultivation, hydrogen evolution through both glucose consumption and decomposition of the extrinsic formate occurred together, while hydrogen evolution occurred only through glucose consumption in the control cultures. The hydrogen evolution rates in the formate cultures were faster than in the control cultures, although cell growth and glucose consumption rates in the formate cultures were slower than the control cultures'. The decomposition rate of the extrinsic formate in the pH 5.8 formate culture was faster than in the pH 6.3 formate culture. The hydrogen yield from glucose in the pH 6.3 formate culture increased due to the increasing amount of the nicotinamide adenine dinucleotide for hydrogen production.

Bioreactors↗
PubMed2005

Therapeutic response to single intravenous bolus administration of formate dehydrogenase in methanol-intoxicated rats.

Methanol remains to be a major public and environmental health hazard. Formic acid is the toxic metabolite responsible for the metabolic acidosis observed in methanol poisoning in humans, in non-human primates and in folate-depleted rodents. Cytochrome oxidase inhibition by formate leads to lactic acid accumulation, which contributes significantly to metabolic acidosis. Toxic effects in human beings are characterized by formic acidemia, metabolic acidosis, ocular toxicity, nervous system depression, blindness, coma and death. Elimination of formate is one of the principles of management in methanol poisoning. Hemodialysis facility is not readily available in all the places, in developing countries like India. Formate dehydrogenase (EC 1.2.1.2) acts directly over formate and converts formate into CO(2) in the presence of NAD. Effect of single intravenous bolus infusion of formate dehydrogenase, obtained from Candida boidinii; in methanol-intoxicated folate deficient rat model was evaluated. Folate depletion induced by methotrexate (MTX) treatment. Carbicarb (Carb) (equimolar solution of sodium carbonate and sodium bicarbonate) was used to treat metabolic acidosis. Experimental design consists of seven groups, namely Saline control, methanol control, MTX control, Enzyme control, MTX-methanol control, MTX-methanol-Carb and MTX-methanol-Carb-Enz group. Male wistar rats treated with MTX (0.3mg/kg) for a week, were injected (i.p.) with methanol (4 gm/kg), 12h latter, Carbicarb solution was infused, following this enzyme was infused (i.v.) in bolus. Blood samples were collected every 15 min for an hour from the cannulated left jugular vein and blood methanol, formate were estimated, respectively, with HPLC and fluorimetric assay. Blood pH, blood gases pO(2), pCO(2) and bicarbonate were monitored with blood gas analyzer in order to evaluate acid base status of the animal. Results obtained show that there is significant elimination of formate within 15 min. It may be concluded that single bolus infusion of formate dehydrogenase facilitates fast removal of formate, a highly toxic metabolite in methanol poisoning.

Acidosis↗
PubMed1987

Formate in urine as a biological indicator of formaldehyde exposure: a review.

The presence of a small amount of endogenously derived formate in human urine is normal; however, formate derived from the metabolism of formaldehyde, several other industrial compounds and some pharmaceuticals may elevate the urine formate concentration above the normally expected values. This elevation in the urine formate concentration presents the possibility of using this as a tool for monitoring exposure to chemicals. Unfortunately, the use of urine formate as a technique for monitoring personal chemical exposure has yet to be evaluated. This review identifies several potentially important variables that could alter the extent to which formate is eliminated through the urine and that could affect the accuracy of using urine formate concentration as an indicator of chemical exposure. Some potentially important confounders that have been identified, but not evaluated adequately, include dietary intake, nutritional status and exposure to cigarette smoke. Furthermore, the metabolism and elimination kinetics have yet to be adequately demonstrated in humans. Without having controlled for potential confounders in previous pharmacokinetic studies, it is unknown whether or not the large range and variation observed in human studies is due to the confounders or to innate individual variability. Given the poor understanding of the normal variation of formate concentration in the urine, the use of it as a biological indicator of chemical exposure becomes questionable. Without appreciable skin penetration, as in this case, the reliance upon air monitoring alone may be more practical. The evidence at this time suggests that the use of urine formate to monitor chemical exposure offers a broad opportunity for investigative research. At the present time, however, the interpretation of urine formate concentration in samples obtained from workers would be difficult.

Animals↗
PubMed2005

Increased serum formate in the diagnosis of methanol poisoning.

Early diagnosis is essential for successful treatment in methanol poisoning. Methanol detection by gas chromatography is not available in most hospitals. Methanol increases the osmolal gap in serum and its metabolite formate increases the anion gap. The sensitivity of these indirect diagnostic methods is not good at low concentrations of methanol or formate. We therefore studied the usefulness of formate measurement in diagnosing methanol poisoning. In 15 patients poisoned with methanol, serum formate was measured enzymatically on a Cobas Mira analyzer using formate dehydrogenase and nicotinamid adenine dinucleotid. Day-to-day coefficient of variation was 5%, and the upper reference limit was 2 mg/dL (0.4 mmol/L). Methanol was detected in all 15 patients of whom 14 had elevated serum formate concentrations. Anion gap was increased in 11 of 11, and osmolal gap in 11 patients of 15 examined. Metabolic acidosis was present in 12 of 15 patients, but pH was below 7.30 in only 9 of them. Four patients with no symptoms had formate concentrations in the range 2-38 mg/dL (0.5-8.3 mmol/L), indicating that increased serum formate was a sensitive indicator of methanol poisoning. Our results proved formate analyzes to be a simple, sensitive, and specific way of diagnosing methanol poisoning. Confounders are patients admitted early, or concomitant ethanol ingestion, and therefore no acidosis. This problem may, however, be omitted by repeated formate analysis in patients developing metabolic acidosis.

Adult↗
PubMed1992

NADH formation by Na(+)-coupled reversed electron transfer in Klebsiella pneumoniae.

Citrate is fermented by Klebsiella pneumoniae to 2 acetate, 0.5 formate and 1.2 CO2. The formation of less than 1 formate and greater than 1 CO2 per citrate can be accounted for by the oxidation of formate to CO2 in order to provide reducing equivalents for the assimilation of citrate into cell carbon. A membrane-bound electron transport chain is apparently involved in NADH synthesis by these cells. The electrons from formate oxidation to CO2 are used to reduce ubiquinone to ubiquinol by membrane-bound formate dehydrogenase and ubiquinol further delivers its electrons to NAD+, if this endergonic reaction is powered by delta mu Na+. The endogenous NADH level of K. pneumoniae cells thus increased in the presence of formate in response to a delta pNa+ greater than -100 mV. NADH formation was completely abolished in the presence of oxygen or after addition of hydroxyquinoline-N-oxide, a specific inhibitor of the Na(+)-translocating NADH:ubiquinone oxidoreductase. The increase of endogenous NADH was dependent on the delta pNa+ applied to the cells. Inverted membrane vesicles of K. pneumoniae catalysed the reduction of NAD+ to NADH with formate as electron donor after application of delta mu Na+ of about 120 mV consisting of delta pNa+ of 60 mV and delta psi of the same magnitude. Neither the delta pNa+ nor the delta psi of this size alone was sufficient to drive the endergonic reaction. Strictly anaerobic conditions were required for NADH formation and hydroxyquinoline-N-oxide completely inactivated the reaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Citrates↗
PubMed1970

Formate as an intermediate in the bovine rumen fermentation.

An average of 11 (range, 2 to 47) mumoles of formate per g per hr was produced and used in whole bovine rumen contents incubated in vitro, as calculated from the product of the specific turnover rate constant, k, times the concentration of intercellular formate. The latter varied between 5 and 26 (average, 12) nmoles/g. The concentration of formate in the total rumen contents was as much as 1,000 times greater, presumably owing to formate within the microbial cells. The concentration of formate in rumen contents minus most of the plant solids was varied, and from the rates of methanogenesis the Michaelis constant, K(m), for formate conversion to CH(4) was estimated at 30 nmoles/g. Also, the dissolved H(2) was measured in relation to methane production, and a K(m) of 1 nmole/g was obtained. A pure culture of Methanobacterium ruminantium showed a K(m) of 1 nmole of H(2)/g, but the K(m) for formate was much higher than the 30 nmoles for the rumen contents. It is concluded that nonmethanogenic microbes metabolize intercellular formate in the rumen. CO(2) and H(2) are the principal substrates for rumen methanogenesis. Eighteen per cent of the rumen methane is derived from formate, as calculated from the intercellular concentration of hydrogen and formate in the rumen, the Michaelis constants for conversion of these substrates by rumen liquid, and the relative capacities of whole rumen contents to ferment these substrates.

Animals↗
PubMed1969

Nitrate reductase complex of Escherichia coli K-12: participation of specific formate dehydrogenase and cytochrome b1 components in nitrate reduction.

The participation of distinct formate dehydrogenases and cytochrome components in nitrate reduction by Escherichia coli was studied. The formate dehydrogenase activity present in extracts prepared from nitrate-induced cells of strain HfrH was active with various electron acceptors, including methylene blue, phenazine methosulfate, and benzyl viologen. Certain mutants which are unable to reduce nitrate had low or undetectable levels of formate dehydrogenase activity assayed with methylene blue or phenazine methosulfate as electron acceptor. Of nine such mutants, five produced gas when grown anaerobically without nitrate and possessed a benzyl viologen-linked formate dehydrogenase activity, suggesting that distinct formate dehydrogenases participate in the nitrate reductase and formic hydrogenlyase systems. The other four mutants formed little gas when grown anaerobically in the absence of nitrate and lacked the benzyl viologen-linked formate dehydrogenase as well as the methylene blue or phenazine methosulfate-linked activity. The cytochrome b(1) present in nitrate-induced cells was distinguished by its spectral properties and its genetic control from the major cytochrome b(1) components of aerobic cells and of cells grown anaerobically in the absence of nitrate. The nitrate-specific cytochrome b(1) was completely and rapidly reduced by 1 mm formate but was not reduced by 1 mm reduced nicotinamide adenine dinucleotide; ascorbate reduced only part of the cytochrome b(1) which was reduced by formate. When nitrate was added, the formate-reduced cytochrome b(1) was oxidized with biphasic kinetics, but the ascorbate-reduced cytochrome b(1) was oxidized with monophasic kinetics. The inhibitory effects of n-heptyl hydroxyquinoline-N-oxide on the oxidation of cytochrome b(1) by nitrate provided evidence that the nitrate-specific cytochrome is composed of two components which have different redox potentials but identical spectral properties. We conclude from these studies that nitrate reduction in E. coli is mediated by the sequential operation of a specific formate dehydrogenase, two specific cytochrome b(1) components, and nitrate reductase.

Cytochromes↗
PubMed2026

Comprehensive transcriptomics and proteomics analysis of neointima formation in human saphenous vein: implications for bypass graft disease.

Human saphenous veins (SVs) are widely used as grafts in coronary artery bypass (CABG) surgery but often fail due to neointima formation. Little is known, however, regarding the cellular, transcriptomic, and proteomic dynamics of neointima formation in human veins. Here, we performed transcriptomics and proteomics analysis in an ex vivo tissue culture model of neointima formation in human SVs procured for CABG surgery. Histological examination demonstrated significant elastin degradation and neointima formation (indicated by increased neointima area and neointima-to-media ratio) in SVs subjected to tissue culture. Analysis of data from 72 patients suggests that the progression of SV remodeling and neointima formation differs according to sex and body mass index, which is negatively associated with neointima formation in males only. RNA sequencing demonstrated upregulation of proinflammatory and proliferation-related genes during neointima formation and identified novel processes, including increased cellular stress and DNA damage responses, reflecting tissue trauma associated with vein harvesting. Proteomic analysis identified upregulated extracellular matrix-related and coagulation/thrombosis proteins and downregulated metabolic proteins. Spatial transcriptomics, used to infer regionally enriched gene expression, suggested dynamic alterations in fibroblast and vascular smooth muscle cell (VSMC) states during neointima formation. Specifically, we identified the emergence of HES1+ and matrix metalloproteinase 2- and 14-positive (MMP2+/MMP14+) expression in VSMCs and fibroblasts, respectively, during neointima formation. Furthermore, our data suggest that MIR647, identified through screening, maintains VSMC contractile gene expression. Our findings suggest dynamic transcriptomic and proteomic changes during neointima formation in human veins and provide useful mechanistic information for the pathogenesis of SV graft disease.NEW & NOTEWORTHY Using multiomics and spatial transcriptomics, we uncover dynamic molecular and cellular changes driving neointima proliferation in human saphenous veins, the most common conduit for bypass surgery. Our study highlights sex- and body mass index-associated differences, novel fibroblast and smooth muscle cell states, and a role for microRNA-647 in preserving vascular contractile phenotype. These findings provide new insight into the mechanisms of vein graft failure and may guide future strategies to improve coronary bypass outcomes.

Humans↗
PubMed1996

Mechanism of H(+)-coupled formate transport in rabbit renal microvillus membranes.

It has been proposed that a major fraction of Cl- absorption in the mammalian proximal tubule occurs by Cl-/formate exchange across the apical membrane with recycling of formate by nonionic diffusion. The purpose of this study was to characterize the mechanism of formate recycling in rabbit renal microvillus membrane vesicles. Formate uptake was stimulated by an inside-alkaline pH gradient. When external pH (pH alpha) was varied at constant internal pH (pHi), the initial rate of formate uptake was less than predicted for nonionic diffusion of formic acid at constant formic acid permeability. When pHi was varied at constant pHi, the initial rate of formate uptake exhibited cooperative and saturable kinetics with respect to pHi, in contrast to the pHi independence predicted for nonionic diffusion. pH gradient-stimulated [14C]formate uptake was stimulated by internal formate, indicating formate/formate exchange. pH gradient-stimulated formate influx was sensitive to inhibition by 1 mM 4,4'-diisothiocyanostilbene-2, 2'-disulfonic acid but not by furosemide or hydroxycinnamate. We conclude that pH gradient-stimulated formate uptake takes place by a carrier-mediated process of H(+)-formate cotransport, OH-/formate exchange, or facilitated formic acid diffusion, rather than solely by passive nonionic diffusion through the lipid bilayer.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗