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PubMed2002

Treatment of compulsive sexual behaviour with naltrexone and serotonin reuptake inhibitors: two case studies.

Although there is no universally accepted definition of compulsive sexual behaviour (CSB), the term is generally used to indicate excessive sexual behaviour or sexual cognitions that lead to subjective distress, social or occupational impairment, or legal and financial consequences. Similar to impulse control disorders, CSB is characterized by a failure to resist the impulse for sex. Opioid antagonists have been effective in treating urge-driven disorders, such as pathological gambling disorder, alcoholism, borderline personality disorder with self-injurious behaviour, cocaine abuse, mental retardation with self-injurious behaviour and eating disorders. Based upon the efficacy of opioid antagonists in treating disorders associated with urges, we hypothesized that naltrexone would reduce both the urges associated with CSB and therefore reduce the sexual behaviour. We present two case reports of individuals with CSB treated successfully with naltrexone, a novel treatment for CSB. In both cases, symptoms dramatically decreased and psychosocial functioning improved with the use of naltrexone. Although more research is needed to determine the mechanism that leads to the excessive sexual behaviour in individuals with CSB, the present case reports suggest that naltrexone may be effective in treating some cases of CSB.

Adult↗
PubMed1999

Two genes from Bacillus subtilis under the sole control of the general stress transcription factor sigmaB.

The general stress response of Bacillus subtilis is triggered by a variety of environmental and metabolic stresses which activate the sigmaB transcription factor. Among the more than 100 genes controlled by sigmaB (the csb genes), the functions identified thus far include resistance to oxidative stress, resistance to protein denaturation and resistance to osmotic stress. To understand the breadth of functions in which csb genes participate, the transcriptional organization and predicted products of two such genes previously identified in a screen for sigmaB-dependent lacZ fusions were analysed. The csb-22::Tn917lacZ and csb-34::Tn917lacZ fusions are unusual among csb genes in that their expression appears to be completely dependent upon sigmaB. By plasmid-integration experiments, fusion analyses and site-directed mutagenesis, stress-inducible, sigmaB-dependent promoters for both these fusions were identified. The csb-34 fusion marked an ORF (yxcC or csbC) which by sequence analysis lay in a monocistronic transcriptional unit. This ORF encoded a predicted 461-residue product which had high identity with Class I sugar transporters of the major facilitator superfamily. It was speculated that the csbC product could serve either a nutritional or an osmotic protection function. In contrast, the csb-22 fusion identified an ORF (ywmG or csbD) which appeared to be the second gene of a two-gene operon. This ORF encoded a predicted 62-residue product which resembled a small Escherichia coli protein of unknown function. The sigmaB. dependent promoter lay immediately upstream from csbD and appeared to be an internal promoter for the operon.

Amino Acid Sequence↗
PubMed2006

Neuroanatomical specificity in the expression of the immediate early gene c-fos following expression of appetitive and consummatory male sexual behaviour in Japanese quail.

We investigated the neural sites related to the occurrence of appetitive (ASB) and consummatory (CSB) aspects of male sexual behaviour in Japanese quail. Castrated males treated with testosterone were exposed for 5 min to one of four experimental conditions: (i) free interaction with a female (CSB group); (ii) expression of rhythmic cloacal sphincter movements in response to the visual presentation of a female (ASB-F group); (iii) or a male (ASB-M group), and (iv) handling as a control manipulation. Brains were collected 90 min after the start of behavioural tests and stained by immunocytochemistry for the FOS protein. An increase in FOS expression was observed throughout the rostro-caudal extent of the medial preoptic nucleus (POM) in CSB males, whereas the view of a female (ASB-F) induced an increased FOS expression in the rostral POM only. In the CSB group, there was also an increase in FOS expression in the bed nucleus striae terminalis, and both the CSB and ASB-F groups exhibited increased FOS expression in aspects of the ventro-lateral thalamus (VLT) related to visual processing. Moreover, both the CSB and ASB-M groups showed increased FOS expression in the lateral septum. These data provide additional support to the idea that there is a partial anatomical dissociation between structures involved in the control of both aspects of male sexual behaviour and independently provide data consistent with a previous lesion study that indicated that the rostral and caudal POM differentially control the expression of ASB and CSB in quail.

Animals↗
PubMed2002

Apnea-related heart rate variability and its clinical utility in congestive heart failure outpatients.

BACKGROUND: Cheyne-Stokes breathing (CSB) is an abnormal cyclical pattern of respiratory fluctuations observed during sleep in congestive heart failure (CHF) of poor prognosis. We examined the clinical usefulness of CSB screening using the heart rate variability (HRV) data from the ambulatory electrocardiogram. METHODS: We monitored ambulatory electrocardiograms and respiration simultaneously in 86 heart disease patients of both sexes, aged 57 +/- 1 years. HRV was analyzed by the maximum entropy method during the sleeping period (11 PM-5 AM). The 43 CHF patients underwent a 1-year follow-up study. RESULTS: In the power spectra of the HRV, peaks were observed within the CSB band (0.005 to 0.03 Hz). Statistically significant differences in HRV were observed between CSB patients and CSB-free patients in very low frequency (VLF) (P = 0.04), VLF/total frequency (TF) (P = 0.02), CSB (P = 0.01), CSB/TF (P = 0.003), and CSB/VLF (P < 0.0001). Cardiac events occurred in 23% of patients, including cardiac death in two, and rehospitalization for aggravated CHF in eight. In a multivariate Cox regression analysis in which age, sex, ejection fraction, NYHA functional class, beta blocker use, and basic heart disease were included, absence of ACE inhibitor use (RR 5.5, 95% CI 1.0-31) and CSB/VLF > or =80% (RR 4.2, 95% CI 1.1-17) remained significant predictors of cardiac events. CONCLUSIONS: HRV can act as an indicator of the presence of CSB in CHF patients, and could therefore be used, under outpatient conditions, to identify a CHF patients with a poor prognosis.

Adrenergic beta-Antagonists↗
PubMed2006

Hydrogen sulfide facilitates carotid sinus baroreflex in anesthetized rats.

AIM: To study effects of hydrogen sulfide (H2S) on the carotid sinus baroreflex (CSB). METHODS: The functional curve of the carotid sinus baroreflex was measured by recording changes in arterial pressure in anesthetized male rats with perfused carotid sinus. RESULTS: H2S (derived from sodium hydrosulfide) at concentrations of 25, 50, and 100 micromol/L facilitated the CSB, shifting the functional curve of the baroreflex downward and to the left. There was a marked increase in peak slope (PS) and reflex decrease in blood pressure (RD). Effects were concentration-dependent. Pretreatment with glibenclamide (20 micromol/L), a K(ATP) channel blocker, abolished the above effects of H2S on CSB. Pretreatment with Bay K8644 (an agonist of calcium channels; 500 nmol/L) eliminated the effect of H2S on CSB. An inhibitor of cystathionine gamma-lyase (CSE), DL-propargylglycine (PPG; 200 micromol/L), inhibited CSB in male rats and shifted the functional curve of the baroreflex upward and to the right. CONCLUSION: These data suggest that exogenous H2S exerts a facilitatory role on isolated CSB through opening K(ATP) channels and further closing the calcium channels in vascular smooth muscle. Endogenous H2S may activate the activity of the CSB in vivo.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Effects of a new molasses byproduct, concentrated separator byproduct, on nutrient digestibility and ruminal fermentation in cattle.

Continuous chromatographic separator techniques have allowed the extraction of more simple sugars from molasses (MOL). The resultant byproduct, concentrated separator byproduct (CSB), has reduced readily fermentable carbohydrates but elevated CP and mineral content. The feed value of CSB was compared to that of MOL in two separate trials. In Trial 1, a chopped forage mixture containing 84% meadow grass hay and 8% alfalfa hay was mixed with either CSB or MOL at 7.3% of DM. Diets were administered to four ruminally cannulated cows in a single reversal design. digestibility of DM, ADF, NDF, and CP were measured. Ruminal pH, ammonia nitrogen (NH3), VFA, total viable bacteria (TVB), cellulose-xylan fermenting bacteria (CXFB), and ciliated protozoa (PTZ) were evaluated. Blood profiles of electrolytes were also measured. Digestibility of DM, ADF, NDF, and CP were 69.03, 68.58; 57.48, 57.77; 65.62, 64.75; and 67.63, 65.07% for the MOL and CSB diets, respectively. Only CP digestibility differed (P less than .02). Ruminal pH, NH3, VFA, TVB, CXFB, and PTZ were 6.97, 6.93; 14.21, 16.71 mg/dL; 74.30, 74.78 mumol/mL; 26.79, 27.36 x 10(9)/mL; 21.72, 21.36%; and 13.90, 7.80 x 10(3)/mL for the MOL and CSB diets, respectively. Ruminal measurements did not differ. Blood electrolyte profiles were not altered. Trial 2 was similar to Trial 1 except the basal diet used was 47% barley grain, 35% alfalfa hay, and 10% barley straw. Either MOL or CSB was added at 7.3% of the DM. Digestibilities of DM, ADF, NDF, and CP were 69.52, 71.33; 35.96, 37.11; 27.93, 33.47; and 71.10, 73.66% for the MOL and CSB diets, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed2000

The relationship between benzo[a]pyrene-induced mutagenesis and carcinogenesis in repair-deficient Cockayne syndrome group B mice.

Cockayne syndrome (CS) patients are deficient in the transcription coupled repair (TCR) subpathway of nucleotide excision repair (NER) but in contrast to xeroderma pigmentosum patients, who have a defect in the global genome repair subpathway of NER, CS patients do not have an elevated cancer incidence. To determine to what extent a TCR deficiency affects carcinogen-induced mutagenesis and carcinogenesis, CS group B correcting gene (CSB)-deficient mice were treated with the genotoxic carcinogen benzo(a)pyrene (B[a]P) at an oral dose of 13 mg/kg body weight, three times a week. At different time points, mutant frequencies at the inactive lacZ gene (in spleen, liver, and lung) as well as at the active hypoxanthine phosphoribosyltransferase (Hprt) gene (in spleen) were determined to compare mutagenesis at inactive versus active genes. B[a]P treatment gave rise to increased mutant frequencies at lacZ in all of the organs tested without a significant difference between CSB-/- and wild-type mice, whereas B[a]P-induced Hprt mutant frequencies in splenic T-lymphocytes were significantly more enhanced in CSB-/- mice than in control mice. The sequence data obtained from Hprt mutants indicate that B[a]P adducts at guanine residues were preferentially removed from the transcribed strand of the Hprt gene in control mice but not in CSB-/- mice. On oral treatment with B[a]P, the tumor incidence increased in both wild-type and CSB-deficient animals. However, no differences in tumor rate were observed between TCR-deficient CSB-/- mice and wild-type mice, which is in line with the normal cancer susceptibility of CS patients. The mutagenic response at lacZ, in contrast to Hprt, correlated well with the cancer incidence in CSB-/- mice after B[a]P treatment, which suggests that mutations in the bulk of the DNA (inactive genes) are a better predictive marker for carcinogen-induced tumorigenesis than mutations in genes that are actively transcribed. Thus, the global genome repair pathway of NER appears to play an important role in the prevention of cancer.

Animals↗
PubMed1981

Influence of cardiac rhythm disturbances and antiarrhythmic drugs on the efflux of PGE, PGF2 alpha, cyclic AMP, and cyclic GMP in canine coronary sinus blood.

In anaesthetized open-chest dogs, cardiac arrhythmias (CA) were induced by cumulative intravenous doses of aconitine or ouabain. Aconitine in a dose which did not induce CA had no influence on the PGE and PGF2 alpha effluxes into coronary sinus blood (CSB), whereas the PGE efflux into CSB increased after a subtoxic dose of ouabain. However, both PGE and PGF2 alpha effluxes were increased, when CA had developed. During aconitine induced CA, the PGE efflux was 6.5-fold and that of PGF2 alpha had increased by 80%. During ouabain induced CA, the effluxes of both PGs were about 3-fold. Propranolol and lidocaine decreased the PGF2 alpha efflux into CSB by about 50% and the PGE efflux was doubled after lidocaine and decreased after propranolol by about a third. The increased PGE efflux into CSB during CA was normalized after propranolol and quinidine if the CA was abolished or the cardiac rhythm improved. Lidocaine did not modify the increase in PGE efflux, despite the abolishment of CA. The increase in PGF2 alpha efflux was not influenced by antiarrhythmic drugs. The cyclic AMP and cyclic GMP in CSB remained unchanged during ouabain induced arrhythmias or after propranolol. The increased efflux of PGE into CSB during aconitine and ouabain induced CA and its abolishment by propranolol support the hypothesis that PGE participates in the modulation of increased sympathetic tone during CA.

Aconitine↗
PubMed1982

Acute toxicity of methanol in the folate-deficient acatalasemic mouse.

Formate acidosis is the chief measurable biochemical characteristic of acute methanol toxicity in man. Its marked elevation in the blood stream of primates has been proposed to account for their much greater susceptibility versus rodents to methanol poisoning. Therefore, a study was undertaken to assess whether folic acid deficient (FAD) mice which accumulate formate are much more sensitive to the lethal effects of this alcohol than folic acid sufficient (FAS) mice. Moreover, because some formate is oxidized by catalase-H2O2 in rodents, but not in primates, we also compared the urinary excretion and blood plasma accumulation of formate and the methanol sensitivity of acatalasemic mice. Methanol-dosed C57BL/6Csb (acatalasemic) mice exhibit slightly lower LD50S than CSa (normal catalase) mice, irrespective of their folate state. CSb-FAD mice excreted much more formate and developed higher plasma formate concentrations (11-17 mM) than identically dosed CSa-FAD animals (6 mM). However, in no instance did a folate deficiency produce a large reciprocal decrease in the oral or i.p. LD50 that would be expected from a huge increase (greater than 10-fold) in the 24-h blood plasma formate level. A low methionine (0.2%) intake did not decrease the oral methanol LD50 of CSb-FAD mice, although excess dietary methionine (1.8%) did lower it from 7.1 to 6.4 g/kg. Methanol treated (4 g/kg) Csb-FAD mice excreted 30.8-48.2% of the oral dose as urinary formate, depending on the level of dietary methionine. Csb-FAS and -FAD mice which were given 2 g/kg sodium formate orally (LD50 = 4.7 and 3.7 g/kg) cleared this dose from the blood within 24 h and excreted 58% and 76% of it, respectively, in the urine. Our results indicate that the plasma formate concentration does not correlate well with methanol lethality in Csb-FAS vs. -FAD mice. In addition, urinary excretion, not oxidation, is the primary means by which mice, and probably rats, eliminate high levels of blood formate. Since the Csb-FAD mouse attains high plasma formate levels and low blood pH-values similar to those which have been reported for methanol poisoned monkeys, it appears to be of value as an inexpensive small animal model for further studies of lethal methanol toxicity and the contribution of formate to this process.

Acatalasia↗
PubMed2005

PKC- and PI3K-dependent but ERK-independent proliferation of murine splenic B cells stimulated by chondroitin sulfate B.

High molecular weight polyanions such as dextran sulfate are known to be weak polyclonal activators of murine B cells, but the molecular mechanism of their mitogenic activitiy is not fully elucidated. Although chondroitin sulfate A (CSA), B (CSB) and C (CSC) are highly charged polyanions, little is known about their effects on the proliferation of B cells. In this study, we demonstrated that CSB stimulated proliferation of murine B cells as markedly as did anti-IgM antibody, more markedly than did dextran sulfate and much more markedly than did CSA, CSC, heparin and hyaluronic acid. CSB caused translocation of protein kinase C (PKC) isoform beta from cytosol to membrane fractions and increased phosphorylation of Akt but not phosphorylation of extracellular signal-regulated kinase (ERK) of B cells. CSB-induced B cell proliferation was almost completely blocked by either the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 or the PKC inhibitor GF109203X but was not significantly inhibited by the ERK kinase inhibitor PD98059. The mitogenic effect of anti-IgM was significantly inhibited by all the three inhibitors, while the mitogenic effect of LPS was inhibited only by LY294002. These findings indicate that CSB stimulated proliferation of murine B cells more markedly than did dextran sulfate and suggest that PKC and PI3K are crucial but that ERK is less important for the mitogenic activity of CSB, the signaling pathways of which may be at least partly distinct from those of anti-IgM and LPS.

Animals↗
PubMed1995

Identification by in Organello footprinting of protein contact sites and of single-stranded DNA sequences in the regulatory region of rat mitochondrial DNA. Protein binding sites and single-stranded DNA regions in isolated rat liver mitochondria.

Footprinting studies with the purine-modifying reagent dimethyl sulfate and with the single-stranded DNA probing reagent potassium permanganate were carried out in isolated mitochondria from rat liver. Dimethyl sulfate footprinting allowed the detection of protein-DNA interactions within the rat analogues of the human binding sites for the transcription termination factor mTERF and for the transcription activating factor mt-TFA. Although mTERF contacts were localized only at the boundary between the 16S rRNA/tRNA(Leu)UUR genes, multiple mtTFA contacts were detected. Contact sites were located in the light and the heavy strand promoters and, in agreement with in vitro footprinting data on human mitochondria, between the conserved sequence blocks (CSB) 1 and 2 and inside CSB-1. Potassium permanganate footprinting allowed detection of a 25-base pair region entirely contained in CSB-1 in which both strands were permanganate-reactive. No permanganate reactivity was associated with the other regions of the D-loop, including CSB-2 and -3, and with the mTERF contact site. We hypothesize that the single-stranded DNA at CSB-1 may be due to a profound helix distortion induced by mtTFA binding or be associated with a RNA polymerase pause site. In any case the location in CSB-1 of the 3' end of the most abundant replication primer and of the 5' end of the prominent D-loop DNA suggests that protein-induced DNA conformational changes play an important role in directing the transition from transcription to replication in mammalian mitochondria.

Animals↗
PubMed1998

Biochemical and biological characterization of wild-type and ATPase-deficient Cockayne syndrome B repair protein.

Cockayne syndrome (CS) is a nucleotide excision repair disorder characterized by sun (UV) sensitivity and severe developmental problems. Two genes have been shown to be involved: CSA and CSB. Both proteins play an essential role in preferential repair of transcription-blocking lesions from active genes. In this study we report the purification and characterization of baculovirus-produced HA-His6-tagged CSB protein (dtCSB), using a highly efficient three-step purification protocol. Microinjection of dtCSB protein in CS-B fibroblasts shows that it is biologically functional in vivo. dtCSB exhibits DNA-dependent ATPase activity, stimulated by naked as well as nucleosomal DNA. Using structurally defined DNA oligonucleotides, we show that double-stranded DNA and double-stranded DNA with partial single-stranded character but not true single-stranded DNA act as efficient cofactors for CSB ATPase activity. Using a variety of substrates, no overt DNA unwinding by dtCSB could be detected, as found with other SNF2/SWI2 family proteins. By site-directed mutagenesis the invariant lysine residue in the NTP-binding motif of CSB was substituted with a physicochemically related arginine. As expected, this mutation abolished ATPase activity. Surprisingly, the mutant protein was nevertheless able to partially rescue the defect in recovery of RNA synthesis after UV upon microinjection in CS-B fibroblasts. These results indicate that integrity of the conserved nucleotide-binding domain is important for the in vivo function of CSB but that also other properties independent from ATP hydrolysis may contribute to CSB biological functions.

Adenosine Triphosphatases↗
PubMed2006

Cockayne syndrome group B protein has novel strand annealing and exchange activities.

Cockayne syndrome (CS) is a rare inherited human genetic disorder characterized by UV sensitivity, severe neurological abnormalities and prageroid symptoms. The CS complementation group B (CSB) protein is involved in UV-induced transcription coupled repair (TCR), base excision repair and general transcription. CSB also has a DNA-dependent ATPase activity that may play a role in remodeling chromatin in vivo. This study reports the novel finding that CSB catalyzes the annealing of complementary single-stranded DNA (ssDNA) molecules with high efficiency, and has strand exchange activity. The rate of CSB-catalyzed annealing of complementary ssDNA is 25-fold faster than the rate of spontaneous ssDNA annealing under identical in vitro conditions and the reaction occurs with a high specificity in the presence of excess non-homologous ssDNA. The specificity and intrinsic nature of the reaction is also confirmed by the observation that it is stimulated by dephosphorylation of CSB, which occurs after UV-induced DNA damage, and is inhibited in the presence of ATPgammaS. Potential roles of CSB in cooperation with strand annealing and exchange activities for TCR and homologous recombination are discussed.

Adenosine Triphosphate↗
PubMed2006

Retinal degeneration and ionizing radiation hypersensitivity in a mouse model for Cockayne syndrome.

Mutations in the CSB gene cause Cockayne syndrome (CS), a DNA repair disorder characterized by UV sensitivity and severe physical and neurological impairment. CSB functions in the transcription-coupled repair subpathway of nucleotide excision repair. This function may explain the UV sensitivity but hardly clarifies the other CS symptoms. Many of these, including retinopathy, are associated with premature aging. We studied eye pathology in a mouse model for CS. Csb(m/m) mice were hypersensitive to UV light and developed epithelial hyperplasia and squamous cell carcinomas in the cornea, which underscores the importance of transcription-coupled repair of photolesions in the mouse. In addition, we observed a spontaneous loss of retinal photoreceptor cells with age in the Csb(m/m) retina, resulting in a 60% decrease in the number of rods by the age of 18 months. Importantly, when Csb(m/m) mice (as well as Csa(-/-) mice) were exposed to 10 Gy of ionizing radiation, we noticed an increase in apoptotic photoreceptor cells, which was not observed in wild-type animals. This finding, together with our observation that the expression of established oxidative stress marker genes is upregulated in the Csb(m/m) retina, suggests that (endogenous) oxidative DNA lesions play a role in this CS-specific premature-aging feature and supports the oxidative DNA damage theory of aging.

Animals↗
PubMed1997

Muscle chemoreflex alters carotid sinus baroreflex response in humans.

The arterial baroreflex opposes pressor responses to muscle ischemia (muscle chemoreflex). Our experiments sought to quantify the unknown effects of muscle chemoreflex on carotid sinus baroreflex (CSB) sensitivity. We generated CSB stimulus-response (S-R) curves by pulsatile application (triggered by each electrocardiogram R wave) of positive and negative neck pressure (from 60 to -80 mmHg in 20-mmHg steps of 20 s each) in seven normal young men. S-R curves were obtained at rest (upright), during the last 3 min of upright cycle ergometer exercise (150 W), and at the first minute of postexercise recovery with leg circulation free (control). A second study repeated the same procedures, except that leg circulation was occluded 20 s before the end of exercise to elicit muscle chemoreflex, and occlusion was maintained during recovery measurements (approximately 3- to 4-min duration). S-R curves for CSB were shifted upward and rightward (25 mmHg) to higher arterial blood pressure (BP) by exercise and less so (10 mmHg) in recovery (free leg flow). Postexercise occlusion (muscle chemoreflex) raised BP and shifted S-R curves above exercise curves. CSB gain rose from -0.26 +/- 0.06 (control) to -0.44 +/- 0.08 (occlusion) during positive neck pressure application and was reduced from -0.14 +/- 0.04 to zero (-0.04 +/- 0.03) during negative neck pressure. Heart rate responses during postexercise muscle chemoreflex were not significantly different from control. Results reveal a nonlinear summation of CSB and muscle chemoreflex effects on BP. BP-raising capability of muscle chemoreflex enhances CSB responses to hypotension but overpowers baroreflex opposition to hypertension.

Adolescent↗
PubMed2002

Oscillations in peripheral arterial tone in congestive heart failure patients: a new marker for Cheyne-Stokes breathing.

Cheyne-Stokes breathing (CSB), which is a prevalent finding in congestive heart failure (CHF) patients, has been shown to be of prognostic value. The oscillations in respiration were shown to be associated with oscillations in sympathetic nerve activation. We tested the hypothesis that the peripheral arterial tone (PAT) as measured by a novel finger plethysmograph can be used to detect CSB. Using a novel technique to measure the PAT, we monitored 10 patients with advanced CHF simultaneously with conventional polysomnographic recordings for either 1 or 2 nights. Records were scored for CSB during 3-min periods based on either respiratory effort and nasal-buccal airflow or on the PAT signal alone. The PAT sensitivity and specificity for the detection of periods containing CSB were 91 and 91% for the entire recording, 90.7 and 92.9% for non-REM sleep, 90.7 and 70% for REM sleep, and 73 and 97.3% for awake periods, respectively. PAT is a reliable marker of CSB in CHF patients. The novel finger plethysmograph can be used for screening and monitoring CSB.

Adult↗
PubMed1999

Prospectively randomized evaluation of stentless versus conventional biological aortic valves: impact on early regression of left ventricular hypertrophy.

BACKGROUND: The aim of this prospectively randomized study was to evaluate left ventricular hypertrophy and its regression after stentless versus conventional biological aortic valve replacement. METHODS AND RESULTS: From March 1996 through April 1998, 180 patients were prospectively selected; 106 patients received a stentless aortic valve (SAV), and 74 received a conventional stented bioprosthesis (CSB). Of these patients, 95% and 96%, respectively, had aortic stenosis. Their mean age was 72.3 and 74.8 years, and there were no significant differences in left ventricular function, preoperative pressure gradients, and NYHA functional status. Aortic annulus diameter indexes were comparable at 13.46 (SAV) versus 13.55 (CSB) mm (P=NS). Larger SAVs were implanted because of the oversizing technique. In-hospital mortality (n=3 and 1 for SAV and CSB) was not valve related. At follow-up, all patients were in NYHA class 1 or 2. Baseline end-diastolic left ventricular posterior wall thickness was 15.6 (SAV) and 14.8(CSB) mm (P=NS) and decreased to 11. 8 (SAV) and 13.2 (CSB) mm (P<0.05) at 6 months. Left ventricular mass index was 213 and 202 g/m(2) at baseline (P=NS), whereas after 6 months, it was 141 (SAV) and 170 (CSB) g/m(2) (P<0.05). CONCLUSIONS: Regression of left ventricular hypertrophy occurs in all patients after aortic valve replacement but is significantly enhanced after SAV implantation. This possibly is due to improved transvalvular hemodynamics.

Aged↗
PubMed1976

The glycosaminoglycans of the human artery and their changes in atherosclerosis.

The changes in levels of glycosaminoglycans (GAGs) of the intima and media of the human artery in atherosclerosis were determined by a recently introduced two-dimensional electrophoresis technique that permits direct measurments of each of these macromolecules. To identify the arterial GAGs, they were fractionated by chromatography on a DEAE-Sephadex A-25 column, and the resulting three fractions (hyaluronic acid [HA], heparan sulfate [HS], and the partially separated chondroitin sulfates B [CSB] and C [CSC]) were analyzed for their electrophoretic mobilities by this electrophoretic method, for their digestability by highly specific hydrolases (leech hyaluronidase, heparinase, and chondroitinases ABC and AC) and for their iduronic acid content. From these studies we concluded that normal and atherosclerotic human aortas contain CSB, CSC, HA, and HS. Further, we demonstrated that CSB is a hybrid consisting of approximately 40% CSA and 60% CSB and that CSC appears to be a polymer consisting essentially of glucuronic acid and N-acetylgalactosamine-6-sulfate. Classical CSA as well as chondroitin (CH) were not present in detectable amounts. In the relatively normal intima, the mean concentrations of the GAGs were found to be 4.7, 20.9, 1.3, and 5.1 mg/g of dry, defatted, decalcified tissue for CSB, CSC, HA, and HS, respectively. With the progression of atherosclerosis, there was a pronounced decrease in the total GAG content (from 32 to 18 mg) associated with a decrease in the CSC and HS levels but without a change in the HA concentrations. Of particular interest, however, was the increase in the CSB level. In the media whose total GAG content averaged approximately 20 mg, no significant changes in these GAG levels were noted with the progression of the disease except for that of CSC. These findings may be important in explaining the increased lipoprotein and collagen deposition in the diseased aorta.

Aorta↗