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PubMed2004

N-acetyl-cysteine accelerates transfer of diabetes into non-obese diabetic scid mice.

AIMS/HYPOTHESIS: Type 1 diabetes mellitus is caused by autoimmune pancreatic beta cell destruction, and the destructive process involves several molecular mechanisms including oxygen-reactive species. A cysteine derivative, N-acetyl-cysteine, is widely used as an antioxidant, but the role of N-acetyl-cysteine in the protection of pancreatic beta cells in type 1 diabetes remains unclear. The aim of this study was to clarify the effect of N-acetyl-cysteine on beta cells using an adoptive transfer system in a murine model of type 1 diabetes. METHODS: Splenocytes from diabetic female non-obese diabetic mice were transferred into female non-obese diabetic scid/ scid recipients to induce diabetes. Just after transfer, N-acetyl-cysteine was administered to non-obese diabetic scid recipients. Two weeks after transfer, the pancreas of the recipients was examined histologically, and cytokine mRNA expression in the pancreas was analysed. In vitro, CD4-positive splenocytes from diabetic donor mice were stimulated with anti-CD3 and anti-CD28 antibodies with or without N-acetyl-cysteine. RESULTS: Treatment with N-acetyl-cysteine significantly accelerated the transfer of diabetes into non-obese diabetic scid recipients. Treatment with N-acetyl-cysteine accelerated the infiltration of mononuclear cells accompanied by CD8-positive cells into the intra-islet region of the recipient's pancreas, and enhanced interferon-gamma mRNA expression in the pancreas. In vitro, treatment with N-acetyl-cysteine enhanced interferon-gamma and interleukin-2 production by CD4-positive splenocytes of the diabetic donor mice. CONCLUSIONS/INTERPRETATION: N-acetyl-cysteine accelerates the transfer of diabetes into non-obese diabetic scid mice and this effect is accompanied by the promotion of local infiltration and T-helper cell type 1 responses.

Acetylcysteine↗

PubMed2006

The chemokine (C-X-C motif) receptor 4 inhibitor AMD3100 accelerates blood flow restoration in diabetic mice.

AIMS/HYPOTHESIS: Bone marrow cell mobilisation potently induces vascular growth in ischaemic tissue, possibly by mobilising endothelial cell progenitors. Thus, mobilising agents might not be therapeutic when endothelial cell progenitors are dysfunctional, as in diabetes mellitus. Local injection of autologous endothelial cell progenitors also stimulates vascular growth in ischaemic tissue, but endothelial cell progenitors from people with multiple cardiovascular risk factors and from obese diabetic mice are marginally therapeutic or inhibitory. We sought to identify possible strategies to improve vascularisation in patients with diabetes mellitus by determining if (1) mobilisation accelerates neovascularisation in diabetic animals, and (2) mobilised cells from a non-diabetic source accelerate vascularisation in diabetic animals. METHODS: We tested whether systemic administration of the chemokine (C-X-C motif) receptor 4 inhibitor AMD3100 or local injection of human CD34(+) circulating cells mobilised by AMD3100 could speed or enhance blood flow restoration in ischaemic limbs of diabetic mice. The small-molecule-mobilising drug AMD3100 was selected because mobilisation and apheresis can be done on the same day. RESULTS: Systemic administration of AMD3100 and local injection of cells mobilised by AMD3100 greatly accelerated the restoration of blood flow to ischaemic limbs of diabetic mice. CD34(+) cells mobilised by AMD3100 appeared to be more potent growth stimulators than their unmobilised counterparts. CONCLUSIONS/INTERPRETATION: Unlike other mobilising agents requiring multi-day mobilisation, AMD3100 enables mobilised donors to undergo mobilisation and apheresis on the same day. The combination of excellent therapeutic benefits as well as ease of use indicates that AMD3100 could be a powerful tool to ameliorate tissue ischaemia in the diabetic environment.

Animals↗

PubMed1998

Apoptosis and beta-cell destruction in pancreatic islets of NOD mice with spontaneous and cyclophosphamide-accelerated diabetes.

Autoimmune-mediated destruction of pancreatic islet beta cells leads to insulin-dependent diabetes in non-obese diabetic (NOD) mice. Although both direct cytotoxic T cell- and indirect cytokine-, nitric oxide- or free radical-mediated mechanisms induce beta-cell apoptosis in vitro, beta-cell death in vivo in spontaneous autoimmune diabetes is not well-characterized. Furthermore, whether beta cells die gradually, or rapidly in the late pre-clinical stage, is a question of current interest. To investigate beta-cell death in vivo, we measured the frequency and intra-islet localisation of apoptosis, defined as DNA strand breaks by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) technique, during spontaneous and cyclophosphamide-accelerated diabetes in NOD mice. In spontaneous diabetes, the frequency of apoptosis in islets correlated with the progression of beta-cell destruction with age. Although apoptosis was detected at low frequency within the reduced insulin-positive islet area of pre-diabetic mice at 90 days of age, it was rarely co-localised to beta cells. After acceleration of beta-cell destruction with cyclophosphamide, the frequency of apoptosis reached maximum at 12 days, at which time 3.2 % of apoptotic cells were beta cells. Apoptosis was most frequent in the insulin-negative islet area comprised of mononuclear cell infiltrate and was localized to CD8+ T cells. The rarity of detectable apoptotic beta cells in spontaneous pre-diabetic mice with pronounced insulitis and reduced insulin-positive islet areas most likely reflects the rapid clearance of apoptotic beta cells. Our findings are more consistent with gradual destruction of non-renewable beta-cells in spontaneous diabetes, than with their rapid, accelerated destruction (as after cyclophosphamide) in the late pre-clinical stage.

Aging↗

PubMed1998

Hitting moving targets. Continuous control of the acceleration of the hand on the basis of the target's velocity.

Previous studies on how we hit moving targets have revealed that the direction in which we move our hand is continuously adjusted on the basis of the target's perceived position, with a delay of about 110 ms. In the present study we show that the acceleration of the hand is also under such continuous control. Subjects were instructed to hit moving targets (running spiders) as quickly as possible with a rod. We found that changing the velocity of the target influenced the speed with which the rod was moved. The influence was noticeable about 200 ms after the target's velocity changed. The extent of the influence was consistent with a direct dependence of the acceleration of the hand on the target's velocity. We conclude that the acceleration of the hand is continuously adjusted on the basis of the speed of the target, with a delay of about 200 ms.

Animals↗

PubMed1999

Genetic typing of the senescence-accelerated mouse (SAM) strains with microsatellite markers.

The Senescence-Accelerated Mouse (SAM) strains constitute a murine model of accelerated senescence originating from the ancestral AKR/J strains and consist of nine senescence-prone (SAMP) strains and four senescence-resistant (SAMR) strains. The chromosomes (Chrs) of the SAM strains were typed with 581 microsatellite markers amplified by PCR, and the fundamental genetic information of the SAM strains was obtained. One-third of the examined markers displayed polymorphism among the strains, and only two alleles were detected in almost all loci among the SAM and AKR/J strains. However, in 12 loci (5.6% of total 215 polymorphic markers), the third allele was detected among the SAM strains. The genetic typing and developmental history suggested that the SAM strains were related inbred strains developed by the accidental crossing between the AKR/J strain and other unknown strain(s). Comparison of the distribution of the loci in the SAMP and the SAMR series revealed notable differences in the four regions on Chrs 4, 14, 16, and 17. This indicated that some of these chromosomal sites might contain the genes responsible for accelerated senescence in the SAMP series.

Aging↗

PubMed2001

Accelerated hyperfractionated radiotherapy with concurrent chemotherapy in locally advanced nasopharyngeal carcinoma: a phase II study.

PURPOSE: The incidence of nasopharyngeal carcinoma in Germany is relatively low in comparison with certain regions in south-east Asia. However, standardised therapeutical regimes are required in the treatment of these tumours. METHODS: Between August 1990 and December 1997, 25 patients with stage III and IV nasopharyngeal carcinoma received an accelerated and hyperfractionated radiotherapy with concurrent chemotherapy (5-FU and mitomycin C). The primary tumour and positive lymph nodes received a total dose of 72 Gy over a period of 6 weeks. In the first 3 weeks, irradiation fields were treated five times per week with 2 Gy per fraction. Thereafter, treatment was accelerated, giving two daily fractions of 1.4 Gy. Salvage surgery was offered for residual lymph node disease after radiotherapy. RESULTS: The overall response rate defined as complete and partial response of the primary was 100%. Sixteen of the 25 patients were still alive and were free of any evidence of tumour recurrence or distant metastases at a mean follow-up period of 34 months (range 7-95 months). Six patients received salvage surgery. Only one of these six patients had histologically proven evidence of vital tumour. No severe late complications such as blindness or temporal lobe necrosis were observed. CONCLUSIONS: The presented data are promising and show that the combination of hyperfractionated accelerated radiotherapy and chemotherapy is feasible and effective.

Adult↗

PubMed2005

Prior injury accelerates subsequent wound closure in a mouse model of regeneration.

Tissue regeneration and scarless healing involves the complete replacement and functional restoration of damaged organs and tissues. In this study of the "scarless healing" MRL mouse model, we demonstrate that 2-mm diameter through-and-through holes made in the cartilaginous part of previously injured MRL mouse ears are closed more efficiently, and that the regenerative repair response is significantly accelerated compared with unprimed MRL and control "nonhealer" strains of mice. Accelerated healing was detected both locally and distally from the original site of injury indicating the involvement of systemic components such as circulating cell types or soluble factors. Histologically, we observed early differences during the wound repair process (before Day 4 post injury) with accelerated formation of blastema-like structures, epidermal downgrowths, and enhanced epithelium thickening in wound border zones in primed MRL mice versus unprimed MRL mice. Although the mechanism of tissue regeneration remains unclear, the results from this study justify the use of the MRL model for further experimentation directed toward the identification of proteins and cell types capable of stimulating scarless tissue regeneration.

Animals↗

PubMed2006

The association of anemia and hypoalbuminemia with accelerated decline in GFR among adolescents with chronic kidney disease.

We sought to describe rates of kidney function decline and to identify modifiable risk factors for CKD progression in a multicenter prospective cohort study of adolescents with CKD aged 11 to 18 years seen semiannually for up to three years. Of the 23 subjects meeting inclusion criteria, the average estimated GFR was 51 +/- 27 ml/min/1.73 m(2) (0.85 +/- 0.45 ml/s/1.73 m(2)) at entry. The overall annualized decline in GFR was 5.6 ml/min/1.73 m(2) (0.093 ml/s/1.73 m(2)) per year (95% confidence interval [95% CI]: 1.9 to 9.3 [0.032 to 0.16]). The adjusted annualized decline in GFR was found to be accelerated in males, as well as among those over 15 years of age. The adjusted annualized decline in GFR was greater among those with either anemia (hematocrit below 36%), or hypoalbuminemia (albumin below 4 g/dl [40 g/L]). After adjustment, anemia was associated with an accelerated decline of 7.8 ml/min/1.73 m(2) (0.13 ml/s/1.73 m(2)) (95% CI: 3.3 to 12 [0.055 to 0.20]) and hypoalbuminemia was associated with an accelerated decline of 17 ml/min/1.73 m(2) (0.28 ml/s/1.73 m(2)) (95% CI: 11 to 22 [0.18 to 0.37]). Further study is needed to evaluate whether treatment of anemia or hypoalbuminemia, as outlined in current clinical care guidelines for CKD, may slow the progression of CKD in adolescents.

Adolescent↗

PubMed2003

High-intensity pulsed laser irradiation accelerates bone formation in metaphyseal trabecular bone in rat femur.

Low-energy laser irradiation has positive effects on bone fracture healing, osteoblast proliferation, bone nodule formation, and alkaline phosphatase activity. However, the mechanism by which low-energy laser irradiation affects bone is not clearly known. It was recently found that light at a low radiation dosage is absorbed by intracellular chromophores. High-intensity pulsed laser irradiation can produce acoustic waves in the target surface by rapidly heating the tissue. We considered that the acoustic waves induced by high-intensity pulsed laser irradiation, in addition to the photochemical effects that are induced, accelerate bone formation. To clarify whether high-intensity pulsed laser irradiation accelerates bone formation, we investigated bone formation in the irradiated femur of rat, using histomorphometric analysis. Rat femurs were irradiated with a Q-switched Nd: YAG laser, which has a wavelength of 1064 nm, under two conditions: once a day, with the average fluence rate set at 100 mW/cm(2) (LA1), and twice a day, i.e., every 12 h, with the average fluence rate set at 50 mW/cm(2) (LA2). The mean bone volume and mineral apposition rate in the LA1 group were significantly higher than those in the nonirradiated group (control). These values were highest for the LA2 group, and were about 1.52 and 1.25-fold those of the control, respectively. These data demonstrated that the number of pulses, rather than the intensity of the laser irradiation, affects bone formation. Thus, this study indicated that high-intensity pulsed laser irradiation accelerates bone formation in the metaphysis. This bone formation induced by high-intensity pulsed laser irradiation might be due to laser-induced pressure waves.

Animals↗

PubMed2002

Morphological analysis of skin in senescence-accelerated mouse P10.

Senescence-accelerated mice (SAM) were established as a kind of group of related inbred strains that have been used as animal models for accelerated senescence and age-associated disorders. To analyze the characteristics of skin in SAM, the present study examined its morphology at the histological and ultrastructural levels. Histologic comparison of skin from senescence-accelerated-prone (SAM P10) and -resistant (SAM R1) mice revealed that the most characteristic features of SAM P10 were remarkable increases in the number of mast cells and in the density of collagen fibers in the dermis. Therefore, cutaneous allergic responsiveness and the proliferative activity of fibroblasts were also examined. Ultrastructurally, mast cells in the skin of SAM P10 possessed specific granules which exhibited considerable heterogeneity in electron density and various degrees of degranulation. In contrast, mast cells in the skin of control SAM R1 possessed a population of stable granules. Mast cell granules were frequently in contact with fibroblasts and were in close apposition to collagen fibers in the dermis of SAM P10. The collagen bundles were disorganized, and various diameters of collagen fibers were observed. SAM P10 demonstrated a significantly reduced wheal-and-flare reaction to histamine and tachykinins such as substance P, which suggests that skin aging may cause reduced sensitivity of mast cells and/or blood vessels to extrinsic stimuli. An in-vitro study using organ and monolayer culture demonstrated that the proliferative capacity of fibroblasts in the skin of SAM P10 was reduced in comparison with SAM R1. This is the first report that demonstrates the detailed morphological characteristics of skin in SAM P10. The findings obtained suggest that SAM P10 is a useful animal model of aged human skin, because of its many similar morphological features, including the reduction of the cutaneous allergic response, represented by neurogenic inflammation via the axon reflex, and its decreased fibroblast proliferation.

Aging, Premature↗

PubMed1999

Combination therapy of cholesterol reduction and L-arginine supplementation controls accelerated vein graft atheroma.

Hyperlipidemia contributes to the development of intimal hyperplasia and accelerated atheroma in vein bypass grafts. Dietary cholesterol reduction and oral supplementation with L-arginine have been shown to reduce accelerated atheroma in experimental vein grafts. This study extends these observations by examining the effect of the combination therapy of cholesterol reduction and L-arginine supplementation on the development of intimal hyperplasia in vein grafts in hypercholesterolemic animals. Thirty New Zealand White rabbits had a carotid vein bypass graft performed and were sacrificed at 28 days postoperatively either for morphology (light and electron microscopy) and videomorphometry, or for in vitro contractile studies. Twenty animals received a 1% cholesterol diet for 4 weeks prior to surgery. This diet was continued until harvest in ten animals. Ten cholesterol-fed animals received L-arginine supplementation (2 g/kg/day, p.o.) for 7 days preoperatively and thereafter until harvest and in addition were returned to a normal diet on the day of surgery. The last ten animals were controls (normal diet). Combined cholesterol reduction and L-arginine supplementation prevented accelerated atheroma in vein grafts, halted the change in enhanced smooth muscle cell contractility, and improved endothelial cell function. Early postoperative therapy targeting atheroma development in the high-risk patient could offer significant morphological and functional benefits.

Animals↗

PubMed2006

The contribution of the pleural type 12 interneuron to swim acceleration in Clione limacina.

The pteropod mollusc, Clione limacina, swims by alternate dorsal-ventral flapping movements of its wing-like parapodia. The basic swim rhythm is produced by a network of pedal swim interneurons that comprise a swim central pattern generator (CPG). Serotonergic modulation of both intrinsic cellular properties of the swim interneurons and network properties contribute to swim acceleration, the latter including recruitment of type 12 interneurons into the CPG. Here we address the role of the type 12 interneurons in swim acceleration. A single type 12 interneuron is found in each of the pleural ganglia, which contributes to fast swimming by exciting the dorsal swim interneurons while simultaneously inhibiting the ventral swim interneurons. Each type 12 interneuron sends a single process through the pleural-pedal connective that branches in both ipsilateral and contralateral pedal ganglia. This anatomical arrangement allowed us to manipulate the influence of the type 12 interneurons on the swim circuitry by cutting the pleural-pedal connective followed by a "culture" period of 48 h. The mean swim frequency of cut preparations was reduced by 19% when compared to the swim frequency of uncut preparations when stimulated with 10(-6) M serotonin; however, this decrease was not statistically significant. Additional evidence suggests that the type 12 interneurons may produce a short-term, immediate effect on swim acceleration while slower, modulatory inputs are taking shape.

Animals↗

PubMed2005

Different adaptive traits to cold exposure in young senescence-accelerated mice.

A reduced adaptation to cold is a prominent feature in aged mammals, including humans. The accelerated senescence-prone strain of mice (SAMP) has been studied as an animal model for several age-associated disorders and in the acceleration of senescence. Recent studies revealed that SAMP strains have dysfunctional hyperactive mitochondria and are under a higher oxidative stress status from a young age. To investigate whether young SAMP mice show impaired cold adaptation abilities, we performed cold-exposure experiments. There were no strain differences in baseline body temperature and lowest reached temperature during cold exposure. SAMP1 mice took longer times to reach their lowest temperature in comparison to SAMR1 mice. SAMR1 mice showed an elevation in temperature following cold exposure, whereas SAMP1 mice did not. Behavioral observations demonstrated that SAMP1 mice moved more actively than SAMR1 during cold exposure. However, mRNA levels of uncoupling protein 1 (UCP1), a heat generating protein, as well as plasma norepinephrine levels, were higher in SAMP1 than in SAMR1 mice. This newly found physiological phenotype in SAMP1 mice provides us with a tool to clarify the genetic mechanism which accelerates the senescence process and helps us develop medical means which will bring mankind to a healthy old age.

Adaptation, Physiological↗

PubMed2006

The ACCEL model for accelerating the detoxification kinetics of hydrocarbons requiring initial monooxygenation reactions.

The two-tank accelerator/aerator modification of activated sludge significantly increases the biodegradation of hydrocarbons requiring initial monooxygenation reactions, such as phenol and 2,4-dichlorophenol (DCP). The small accelerator tank has a controlled low dissolved oxygen (DO) concentration that can enrich the biomass in NADH + H+. It also has a very high specific growth rate (mu acc) that up-regulates the biomass's content of the monooxygenase enzyme. Here, we develop and test the ACCEL model, which quantifies all key phenomena taking place when the accelerator/aerator system is used to enhance biodegradation of hydrocarbons requiring initial monooxygenations. Monooxygenation kinetics follow a multiplicative relationship in which the organic substrates (phenol or DCP) and DO have separate Monod terms, while the biomass's content of NADH + H+ has a first-order term. The monooxygenase enzyme has different affinities (K values) for phenol and DCP. The biomass's NADH + H+ content is based on a proportioning of NAD(H) according to the relative rates of NADH + H+ sources and sinks. Biomass synthesis occurs simultaneously through utilization of acetate, phenol, and DCP, but each has its own true yield. The ACCEL model accurately simulates all trends for one-tank and two-tank experiments in which acetate, phenol, and DCP are biodegraded together. In particular, DCP removal is affected most by DOacc and the retention-time ratio, Theta acc/Theta total. Adding an accelerator tank dramatically increases DCP removal, and the best DCP removal occurs for 0.2 < DOacc < 0.5 mg/l and 0.08 < Theta acc/Theta total < 0.2. The rates of phenol and DCP utilization follow the multiplicative relationship with a maximum specific rate coefficient proportional to mu acc. Finally, mu acc increases rapidly for Theta acc/Theta total < 0.25, acetate removal in the accelerator fuels the high mu acc, and the biomass's NADH + H+ content increases very dramatically for DO acc < 0.25 mg/l.

Aerobiosis↗

PubMed2002

Role of 12-lipoxygenase and oxidant stress in hyperglycaemia-induced acceleration of atherosclerosis in a diabetic pig model.

AIMS/HYPOTHESIS: We previously showed that vascular smooth muscle cells and endothelial cells cultured under high glucose conditions produced more 12(S)-hydroxyeicosatetraenoic acid (12-HETE), the 12-lipoxygenase (12-LO) product of arachidonate metabolism, relative to normal glucose. Because the lipoxygenase (LO) pathway has been associated with oxidant stress and the pathogenesis of atherosclerosis, we now examined 12-LO activation in vivo in a pig model of diabetes-induced accelerated atherosclerosis which displays human characteristics. METHODS: The animal model was developed in pigs who were fed a normal or high fat diet and given streptozotocin injections to produce normolipemic-normoglycaemic (NLNG), normolipemic-hyperglycaemic (NLHG), hyperlipemic-normoglycaemic (HLNG) and hyperlipemic-hyperglycaemic (HLHG) pigs. Tissue samples were obtained from key arterial beds to examine 12-LO expression at 20 weeks after the pigs began their diet. RESULTS: All HG pigs maintained threefold higher serum glucose concentrations. The HL groups developed atherosclerosis but diabetic HLHG pigs showed markedly accelerated atherosclerosis (twofold) relative to non-diabetic HLNG pigs. Immunostaining showed progressive increases in 12-LO in arteries in the order NLNG, NLHG, HLNG and HLHG. Leukocyte-type 12-LO protein (immuno-blotting) as well as mRNA expression (by competitive PCR) in abdominal and coronary arteries were significantly greater in HLHG pigs than in all the other three groups. Furthermore, increased oxidant stress was observed in monocytes from NLHG and HLNG pigs, and greatly potentiated in HLHG pigs. CONCLUSIONS/INTERPRETATION: These results are consistent with the hypothesis that 12-LO activation plays a key role in accelerated atherosclerosis due to diabetes and hyperlipemia.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1976

Umbilical vein occlusion and transient acceleration of the fetal heart rate. Experimental observations in subhuman primates.

Transient acceleration of the fetal heart rate is commonly seen in the cardiotachometer tracing of the human fetus during labor. A likely cause appeared to be partial occlusion of the umbilical cord. On the basis of this hypothesis, fetal cardiovascular responses to partial occlusion of the umbilical cord or isolated intra-abdominal portion of umbilical vein were studied in near-term pregnant baboons and rhesus monkeys prior to and following sympathetic blockade with dibenzyline and propranolol. The responses were of two types. In the well-oxygenated fetus, partial occlusion resulted in transient acceleration of heart rate and a decrease in pulse pressure. This response was abolished with dibenzyline or propranolol. In the hypoxic fetus, partial occlusion resulted in either bradycardia and hypotension or hypotension with no alteration in heart rate. Thus, transient acceleration of the fetal heart rate can be explained on the basis of a sympathetic response to diminished venous return. It would appear to be an early sign of a potential cord complication. This response will not be seen if the fetus becomes asphyxiated and hypoxic.

Animals↗

PubMed1979

Fetal heart rate acceleration in labor: excellent prognostic indicator.

This study explores the significance of fetal heart rate acceleration in labor. Fetal heart rate accelerations were studied in 1,677 monitored laboring patients. Fetal outcome was analyzed according to perinatal mortality rate. Apgar scores, and incidence of late deceleration. The presence of accelerations of the fetal heart rate during labor proved to be an excellent indicator of subsequent good fetal outcome.

Apgar Score↗

PubMed1979

Acceleration of the fetal heart rate.

Acceleration of the fetal heart rate during contractions was usually followed by deceleration, and evidence is presented to show that it results from increased sympathetic drive and may be associated with fetal tissue hypoxia. However, the presence of accelerations are not serious and merely warn the obstetrician of the possibility of the occurrence of subsequent decelerations. The mechanism thought most likely to produce accelerations is uterine compression of the umbilical vein during contractions.

Bradycardia↗