PubMed Health⌕ Search

Biomedical subjects

Raymond Coleman

Publications and source records attributed to Raymond Coleman.

At least 37 records · Page 2Linked to original sources
PubMed2004

Omapatrilat decreased macrophage oxidative status and atherosclerosis progression in atherosclerotic apolipoprotein E-deficient mice.

UNLABELLED: Oxidative stress is an important risk factor in the pathogenesis of atherosclerosis. Angiotensin-converting enzyme (ACE) inhibitors attenuate atherosclerosis and oxidative stress in animal models. Omapatrilat, a VasoPeptidase-inhibitor, selectively inhibits both Neutral-Endo-Peptidase (NEP) and ACE. OBJECTIVE: In this study, we analyzed the effect of Omapatrilat administration (1, 4, or 20mg/kg/d, for 12 weeks) to atherosclerotic apolipoprotein E-deficient (E0) mice on their blood pressure (BP), serum and macrophage oxidative status, and atherosclerotic lesion area. RESULTS: Following administration of Omapatrilat (4 mg/kg/d and 20 mg/kg/d), the mice systolic and diastolic BP significantly decreased by up to 33% and 25% respectively, compared with placebo-treated mice. However, administration of Omapatrilat at 1mg/kg/d did not affect the mice BP. The Omapatrilat-treated mice serum susceptibility to lipid peroxidation was reduced by up to 21%, and their serum paraoxonase activity was increased by up to 24%, compared with placebo-treated mice. Peritoneal macrophages from Omapatrilat-treated (20 mg/kg/d) mice exhibited a reduced oxidative stress, evidenced by a reduction in macrophage lipid peroxide content (by 45%), cholesteryl-linoleate hydroperoxide content (by 48%), and oxidized glutathione levels (by 40%). Finally, the area of the mice atherosclerotic lesion was dose-dependently reduced, by 50%, 67%, and 82%, following Omapatrilat administration at 1mg/kg/d, 4 mg/kg/d, and 20 mg/kg/d respectively, compared with placebo-treated mice. CONCLUSION: Omapatrilat has a substantial anti-atherosclerotic effect, which can be related not only to BP reduction but also to its ability to reduce oxidative stress in atherosclerotic E0 mice.

Animals↗
PubMed2004

Impact of a walking program in people with down syndrome.

The purpose of this study was to evaluate the efficacy of a pain-free treadmill walking program in intellectually disabled (ID) adults with arterial occlusive disease. Fourteen participants with mild ID participated in the walking program. Six patients showed stable intermittent claudication. A control (nontreadmill, n = 12) group consisted of 4 individuals with intermittent claudication. Noninvasive determinations of lower-limb hemodynamics included photoplethysmography and ankle-brachial pressure. Pain levels were measured according to a pain pathophysiology index. The treadmill program consisted of individually prescribed low-endurance walking at a 0% incline done at a comfortable speed 3 times per week. All participants completed the 15-week walking program and showed significant improvements (p < 0.05) in walking speed, distance, and duration. Pain levels were reduced in individuals suffering from intermittent claudication. Blood hemodynamic parameters also showed significant improvements. In conclusion, low-intensity treadmill walking significantly improved the functional capacities of adult individuals with mild ID with vascular occlusion and reduced pain levels.

Aged↗
PubMed2003

An experimental platform for studying growth and invasiveness of tumor cells within teratomas derived from human embryonic stem cells.

There is currently no available experimental system wherein human cancer cells can be grown in the context of a mixed population of normal differentiated human cells for testing biological aspects of cancer cell growth (e.g., tumor cell invasion and angiogenesis) or response to anti-cancer therapies. When implanted into immunocompromised mice, human embryonic stem cells develop teratomas containing complex structures comprising differentiated cell types representing the major germ line-derived lineages. We sought to determine whether human cancer cells would grow within such teratomas and display properties associated with malignancy, such as invasiveness and recruitment of blood vessels. HEY ovarian cancer cells stably expressing an H2A-GFP fusion protein (HEY-GFP) injected into mature teratomas developed into tumors, which allowed tracking of tumor cell invasion and recruitment of human teratoma-derived blood vessels. This provides a straightforward and powerful approach to studying the biological properties of cancer cells within the microenvironment of normal differentiated human cells.

Animals↗
PubMed2003

Tissue angiotensin-converting-enzyme (ACE) deficiency leads to a reduction in oxidative stress and in atherosclerosis: studies in ACE-knockout mice type 2.

UNLABELLED: Background- Angiotensin II, produced by angiotensin-converting-enzyme (ACE), enhances oxidative stress and atherogenesis. In this study, we analyzed whether tissue ACE deficiency in ACE-knockout mice type-2 would affect their oxidative status. Moreover, by crossbreeding the ACE-knockout mice with atherosclerotic apolipoprotein E (apo E)-deficient (E0) mice, we questioned whether tissue ACE deficiency affects atherogenesis. METHODS AND RESULTS: ACE-deficient mice type-2 (ACE+/-) exhibited reduced serum lipid peroxidation compared with ACE+/+ mice. Peritoneal macrophages from ACE+/- mice demonstrated lower oxidative status, as exhibited by decreases of 47%, 33% 56%, and 51%, in their lipid peroxides, superoxide release, dichlorofluorescein fluorescence, and LDL oxidation, respectively, compared with ACE+/+ mice. ACE+/- mice crossbred with E0 mice, resulting in atherosclerotic mice heterozygous for ACE (ACE+/-/E0 mice), exhibited reduced lipid peroxidation, increased paraoxonase activity, and lower macrophage LDL oxidation compared with E0 and ACE+/+/E0 mice. ACE+/-/E0 mice also exhibited reduced NADPH-induced aortic superoxide ion production by 52% and a reduction of 43% in their atherosclerotic lesion size compared with E0 mice. Finally, 2 animals genotyped as homozygous-knockout for both ACE and APOE genes (ACE-/-/E0), exhibited a striking reduction of 86% in their atherosclerotic lesion area compared with E0 mice. CONCLUSIONS: Reduction of tissue ACE with the ACE-knockout mouse type-2 model inhibited oxidative stress and atherogenesis.

Animals↗
PubMed2003

Long-term effects of activity status in the elderly on cardiorespiratory capacity, blood pressure, blood lipids, and body composition: a five-year follow-up study.

It is generally recognized that physical activity levels in the elderly do not remain constant over time, and typically there is a marked reduction in physical activities in the elderly. The long-term benefits of regular physical training programs in the elderly are still not fully understood. This is a study of 55 elderly healthy subjects (over 65 years old) and re-evaluated for the effects of different physical activity patterns (sedentary, moderately active, and highly active) on several physiological parameters (pre- and post-training) after a 5-year period (5.30 +/- 1.14 years). Measurements included: body composition, blood lipid profiles, resting systolic and diastolic blood pressure, maximal oxygen uptake, and pulmonary function. Results indicated a larger decrease in maximal oxygen uptake (VO2max) in the group of elderly sedentary individuals (1.5 +/- 0.5 l/min) compared to the moderately active (1.7 +/- 0.6 l/min) and the highly active groups (1.9 +/- 0.4 l/min). An active lifestyle was not sufficient to increase the physiological function of an individual. This study could not clearly demonstrate favorable differences for the physically active groups over the sedentary group with regard to several important physiological factors over the 5-year follow-up and it appears that the recommendation for, and the initiation of, adopting active lifestyles may not be sufficient on their own to significantly increase an individual's physiological functioning.

Aged↗
PubMed2003

Paraoxonase (PON1) deficiency is associated with increased macrophage oxidative stress: studies in PON1-knockout mice.

Human serum paraoxonase (PON1), an HDL-associated esterase, protects lipoproteins against oxidation, probably by hydrolyzing specific lipid peroxides. As arterial macrophages play a key role in oxidative stress in early atherogenesis, the aim of the present study was to examine the effect of PON1 on macrophage oxidative stress. For this purpose we used mouse arterial and peritoneal macrophages (MPM) that were harvested from two populations of PON1 knockout (KO) mice: one on the genetic background of C57BL/6J (PON1(0)) and the other one on the genetic background of apolipoproteinE KO (PON1(0)/E(0)). Serum and LDL, but not HDL, lipids peroxidation was increased in PON1(0), compared to C57BL/6J mice, by 84% and by 220%, respectively. Increased oxidative stress was shown in peritoneal and in arterial macrophages derived from either PON1(0) or PON1(0)/E(0) mice, compared to their appropriate controls. Macrophage oxidative stress was expressed by increased lipid peroxides content in MPM from PON1(0) and from PON1(0)/E(0) mice by 48% and by 80%, respectively, and by decreased reduced glutathione (GSH) content, compared to the appropriate controls. Furthermore, increased capacity of MPM from PON1(0) and PON1(0)/E(0) mice to oxidize LDL (by 40% and by 19%, respectively) and to release superoxide anions was observed. In accordance with these results, PON1(0) mice MPM exhibited 130% increased translocation of the cytosolic p47phox component of NADPH-oxidase to the macrophage plasma membrane, suggesting increased activation of macrophage NADPH-oxidase in PON1(0) mice, compared to control mice MPM. The increase in oxidative stress in PON1-deficient mice was observed despite the presence of the two other members of the PON gene family. PON2 and PON3 activities and mRNA expression were both found to be present in PON1-deficient mice MPM. Upon incubation of PON1(0)/E(0) derived macrophages with human PON1 (7.5 arylesterase units/ml), cellular peroxides content was decreased by 18%, macrophage superoxide anion release was decreased by 33%, and macrophage-mediated oxidation of LDL was reduced by 22%. Finally, a 42% increase in the atherosclerotic lesion area was observed in PON1(0)/E(0) mice, in comparison to E(0) mice under regular chow diet. We thus concluded that PON1 can directly reduce oxidative stress in macrophages and in serum, and that PON1-deficiency results in increased oxidative stress not only in serum, but also in macrophages, a phenomenon that can contribute to the accelerated atherosclerosis shown in PON1-deficient mice.

Animals↗
PubMed2003

Oral insulin supplementation attenuates atherosclerosis progression in apolipoprotein E-deficient mice.

OBJECTIVE: The role of insulin in atherosclerosis progression in diabetes is uncertain. We examined the effects of oral insulin supplementation on atherogenesis in apolipoprotein E-deficient (E(0)) mice. METHODS AND RESULTS: One-month-old male E(0) mice were orally supplemented with human insulin (0.1, 0.5, and 1 U/mL) or placebo for 3 months. At the end of the study, serum and macrophage oxidative stress and atherosclerosis progression were studied. Insulin reduced lesion size by 22% to 37% (P<0.05) in all study groups. Lipid peroxides serum levels were 18% lower (P<0.01), and serum paraoxonase activity was 30% higher (P<0.01) in mice supplemented with 1.0 U/mL insulin compared with controls. Insulin reduced mouse peritoneal macrophage (MPM) lipid peroxides content and superoxide anion release by up to 44% and 62%, respectively (P<0.01). In addition, oral insulin reduced MPM cholesterol content and cholesterol biosynthesis by up to 36% and 53%, respectively (P<0.01). In vitro incubation of E(0) mice MPM with increasing insulin concentrations (0 to 100 micro U/mL) resulted in a dose-dependent reduction of cholesterol synthesis by up to 66% (P<0.05). CONCLUSIONS: In E(0) mice, oral insulin supplementation attenuates the atherosclerotic process. This may be attributable to insulin-mediated reduction of oxidative stress in serum and macrophages as well as reduction in macrophage cholesterol content.

Administration, Oral↗
PubMed2003

Expression of matrix metalloproteinases, inhibitor, and acid phosphatase in muscles of immobilized hindlimbs of rats.

External fixation procedures of limb immobilization provide excellent experimental models to study mechanisms involved in muscle disuse atrophy and recovery. Female Wistar rats (7-8 months old) had their right hindlimbs immobilized by an external fixation procedure for 5, 10, 21, and 30 days. Muscle mass of the gastrocnemius and quadriceps muscles was reduced by 41-46% in comparison with contralateral nonimmobilized legs. Acid phosphatase activities were significantly increased after 21 and 30 days of hindlimb immobilization. Histochemical staining for acid phosphatase activities increased in myofibers after the external fixation and also in macrophages in the adjacent extracellular matrix. Matrix metalloproteinase (MMP-2 and MMP-9) activities assessed by gel zymography and also a tissue inhibitor of metalloproteinases (TIMP-1) assessed by Western blot were elevated in the immobilized hindlimb muscles. Our study demonstrated that metalloproteinases are expressed relatively late after limb immobilization and appear to be responsible to a large degree for degradation of the extracellular matrix in experimental disuse atrophy.

Acid Phosphatase↗
PubMed2003

The aging hand.

Hand function decreases with age in both men and women, especially after the age of 65 years. A review is presented of anatomical and physiological changes in the aging hand. The age-related changes in prehension patterns (grip and pinch strength) and hand dexterity in the elderly population are considered. Deterioration in hand function in the elderly population is, to a large degree, secondary to age-related degenerative changes in the musculoskeletal, vascular, and nervous systems. Deterioration of hand function in elderly adults is a combination of local structural changes (joints, muscle, tendon, bone, nerve and receptors, blood supply, skin, and fingernails) and more distant changes in neural control. These age-related changes are often accompanied by underlying pathological conditions (osteoporosis, osteoarthritis, rheumatic arthritis, and Parkinson's disease) that are common in the elderly population. Assessment of hand function and prehension patterns is needed in order to determine specific treatment approaches.

Activities of Daily Living↗
PubMed2003

Five clinical tests to assess balance following ball exercises and treadmill training in adult persons with intellectual disability.

BACKGROUND: Incidence rates of falling increase progressively with aging. Preventing or delaying the onset of functional decline is a crucial important goal, because more individuals with intellectual disability (ID) are living well into their sixth and seventh decades. The question of whether walking and ball exercises can effect balance performance has never been reported. This pilot study was conducted to determine the effects of therapeutic training on improving balance capabilities in adults with mild ID. METHODS: The study included 13 women and 4 men, aged 50-67 years (mean age 56.5 years) residing in a residential care center. Five clinical tests were used to determine the "real" picture of the locomotor function and balance before and after the training protocol. Baseline values were determined using 2 control groups of age-matched adults with and without ID. The tests included modified get-up-and-go, full turn, forward reach, sit-to-stand, and one-legged standing. Therapeutic training for 6 months included dynamic ball exercises and treadmill walking with a 2-3% positive inclination. RESULTS: Participants in the program showed little to no improvement in terms of their static and dynamic balance compared to their initial values. Thus, only 2 of the tests showed statistical significance. CONCLUSIONS: Lack of improvement was noted in both postural and balance control in adults with mild ID as a result of 6 months of intervention by means of ball exercise and treadmill training.

Aged↗
PubMed2003

Effect of eplerenone, a selective aldosterone blocker, on blood pressure, serum and macrophage oxidative stress, and atherosclerosis in apolipoprotein E-deficient mice.

Oxidative stress is involved in the pathogenesis of atherosclerosis, and angiotensin II (AT-II) induces oxidative stress and enhances atherogenesis. Aldosterone, which has an important role in the pathology of heart failure, has recently been implicated as a mediator of AT-II biologic activities. In this study, we analyzed whether administration of the selective aldosterone blocker eplerenone to atherosclerotic apolipoprotein E-deficient (E0) mice would affect their oxidative status and atherogenesis. Apolipoprotein E-deficient mice were administered chow containing eplerenone (200 mg/kg/day) for 3 months. Blood pressure, serum and macrophage oxidative status, and aortic atherosclerotic lesion area were evaluated in mice treated with eplerenone compared with untreated mice. Eplerenone administration significantly decreased systolic and diastolic blood pressure by 12% and 11%, respectively, compared with untreated mice. Serum susceptibility to lipid peroxidation decreased by as much as 26%, and serum paraoxonase activity increased by 28% in eplerenone-treated mice compared with untreated mice. Peritoneal macrophages from eplerenone-treated mice contained reduced levels of lipid peroxides, and their macrophage oxidation of low-density lipoprotein (LDL) and superoxide ion release were significantly reduced (by 17% and 43%, respectively), compared to untreated mice. Daily injections of AT-II (0.1 mL, 10(-)7M) during the final 3 weeks of the study in eplerenone-treated mice substantially attenuated the eplerenone-mediated reduction in macrophage superoxide release and LDL oxidation. Finally, the atherosclerotic lesion area in aortas of eplerenone-treated mice was significantly reduced (by 35%) versus untreated mice, and this effect was reversed by AT-II. Administration of the selective aldosterone blocker eplerenone significantly reduced oxidative stress and atherosclerosis progression in E0 mice. These data suggest that aldosterone could have a significant pro-oxidative role in the pathogenesis of atherosclerosis.

Aldosterone↗
PubMed2003

Dietary Dunaliella bardawil, a beta-carotene-rich alga, protects against acetic acid-induced small bowel inflammation in rats.

BACKGROUND: Reactive oxygen species mediate tissue injury in inflammatory bowel disease. Beta-carotene is known as a potent free radical quencher and antioxidant. AIM: The authors evaluated the efficacy of prefeeding Dunaliella bardawil, rich in beta-carotene, to ameliorate acid-induced enteritis in a rat model. METHODS: Enteritis was induced in female Sprague-Dawley rats by injection of 2 mL acetic acid (0.67 mol/L) to a ligated duodenal loop following 10 weeks of feeding diets containing beta-carotene and compared with various controls. The effects of beta-carotene were evaluated by changes in myeloperoxidase activity, histology, and histomorphometry. RESULTS: Feeding beta-carotene resulted in suppressed mucosal myeloperoxidase activity, both basal and that induced by acetic acid injection. Acetic acid treatment induced major histopathologic changes in the duodenal mucosa, including small, irregular, and distorted villi; damage to the epithelium; edema of the lamina propria; accumulation of inflammatory cells; and hemorrhage. Beta-carotene treatment prevented these acid-induced histopathologic changes, and this was confirmed by histomorphometry of the villi. CONCLUSIONS: These results demonstrate the effectiveness of beta-carotene in a rat model as a prophylactic dietary measure in reducing the effects of acid-induced enteritis and raise the possibility that patients with Crohn's disease may benefit from the consumption of natural beta-carotene.

Acetic Acid↗
PubMed2003

Assessment of the ultrastructural and proliferative properties of human embryonic stem cell-derived cardiomyocytes.

Assessment of early ultrastructural development and cell-cycle regulation in human cardiac tissue is significantly hampered by the lack of a suitable in vitro model. Here we describe the possible utilization of human embryonic stem cell (ES) lines for investigation of these processes. With the use of the embryoid body (EB) differentiation system, human ES cell-derived cardiomyocytes at different developmental stages were isolated and their histomorphometric, ultrastructural, and proliferative properties were characterized. Histomorphometric analysis revealed an increase in cell length, area, and length-to-width ratio in late-stage EBs (>35 days) compared with early (10-21 days) and intermediate (21-35 days) stages. This was coupled with a progressive ultrastructural development from an irregular myofibrillar distribution to an organized sarcomeric pattern. Cardiomyocyte proliferation, assessed by double labeling with cardiac-specific antibodies and either [3H]thymidine incorporation or Ki-67 immunolabeling, demonstrated a gradual withdrawal from cell cycle. Hence, the percentage of positively stained nuclei in early-stage cardiomyocytes ([3H]thymidine: 60 +/- 10%, Ki-67: 54 +/- 23%) decreased to 36 +/- 7% and 9 +/- 16% in intermediate-stage EBs and to <1% in late-stage cardiomyocytes. In conclusion, a reproducible temporal pattern of early cardiomyocyte proliferation, cell-cycle withdrawal, and ultrastructural maturation was noted in this model. Establishment of this unique in vitro surrogate system may allow to examine the molecular mechanisms underlying these processes and to assess interventions aiming to modify these properties. Moreover, the detailed characterization of the ES cell-derived cardiomyocyte may be crucial for the development of future cell replacement strategies aiming to regenerate functional myocardium.

Cell Differentiation↗
PubMed2002

Ramipril administration to atherosclerotic mice reduces oxidized low-density lipoprotein uptake by their macrophages and blocks the progression of atherosclerosis.

Foam cell formation, the hallmark of early atherosclerosis, results from cholesterol accumulation in arterial macrophages. Angiotensin-II stimulates foam cell formation and angiotensin converting enzyme (ACE) inhibitors reduce atherosclerosis in animal models. The goal of the present study was to determine the effect of the ACE inhibitor Ramipril on the progression of atherosclerosis in apolipoprotein-E-deficient (E0) mice with already advanced atherosclerosis. Therefore, 4-month-old atherosclerotic E0 mice were treated with Ramipril for 2 and 4 months and compared to age-matched placebo-treated mice, as well as to control young (4-month-old) non-treated E0 mice, for their atherosclerosis. Histomorphometry showed that Ramipril treatment substantially inhibited atherogenesis as shown by 48 and 72% reduction in lesion size at 6 and 8 months of age, respectively, compared to the lesion size in age-matched placebo-treated mice. Moreover, the size of the atherosclerotic lesions in 6- and 8-month-old Ramipril-treated mice was almost identical to the size of atherosclerosis of the 4-month-old control mice. Moreover, Ramipril treatment of E0 mice, significantly reduced oxidized low-density lipoprotein (Ox-LDL) uptake by their peritoneal macrophages (MPM) by 32%, compared to Ox-LDL uptake by MPM from 6-month-old placebo mice, and even reduced it by 12% in comparison to Ox-LDL uptake by MPM from 4-month-old control mice. A significant decrease in the mRNA levels of the Ox-LDL receptor CD36 by 58% was observed in macrophages from 6-month-old Ramipril-treated mice compared to macrophages from the 6-month-old placebo-treated mice. There was even a significant reduction (by 32%) in CD36 mRNA levels in macrophages from the 6-month-old Ramipril-treated mice, compared to the CD36 mRNA levels in macrophages from the 4-month-old control mice. We thus conclude that administration of the ACE inhibitor Ramipril to E0 mice, which already exhibit significant atherosclerosis, blocked the progression of the atherosclerotic lesion build-up, a phenomenon that could be related to Ramipril-induced inhibition of Ox-LDL uptake by macrophages.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Increased macrophage glutathione content reduces cell-mediated oxidation of LDL and atherosclerosis in apolipoprotein E-deficient mice.

We used the apolipoprotein E deficient (apo e-/-) mice to analyze the role of macrophage reduced glutathione (GSH) content in cell-mediated oxidation of LDL and in atherosclerotic lesion development. Apo e-/- mice were supplemented with L-2-oxo-4-thiazolidin carboxylate (OTC, which supplies cysteine residues, 500 mg/kg/day), or with buthionine sulfoximine (BSO, a specific inhibitor of GSH synthesis, 400 mg/kg/day) for 6 weeks. Then mouse peritoneal macrophages (MPM) and the mice aortas were collected. MPM from apo e-/- mice contained decreased GSH levels (by 58%), and a four-fold increased lipid peroxides content compared to control macrophages from C57BL6 mice. These MPM demonstrated increased capability to release superoxide anions and to oxidize LDL in comparison to control MPM. OTC supplementation resulted in a 26% increase in macrophage GSH, paralleled by a 25% reduction in cellular lipid peroxides content. Decrement by 30% in superoxide anion release and LDL oxidation by MPM, and also in the atherosclerotic lesion size by 25%, was found in the OTC-treated mice, compared to placebo-treated apo e-/- mice. In contrast, in BSO-treated mice MPM a further depletion of cellular GSH by 22% was found, paralleled by a two-fold increase in lipid peroxides content, and a 41% increased superoxide anion release and cell-mediated LDL oxidation, compared to placebo-treated apo e-/- mice MPM. Most important, BSO supplementation to apo e-/- mice caused a 59% increase in the atherosclerotic lesion area. An additional way to increase cellular GSH content was the use of dietary antioxidants. Vitamin E (40 mg/kg/day) or the isoflavan glabridin (25 microg/kg/day) administration for 2 months to apo e-/- mice resulted in the accumulation of these antioxidants in their MPM, and increased MPM GSH content by 24 and 80%, respectively. MPM lipid peroxides content was reduced by 31 or 60% upon vitamin E or glabridin supplementation, paralleled by a 30 or 60% decrease in cell-mediated oxidation of LDL, respectively. Finally, a significant inverse correlation (R=0.83) was found between macrophage GSH content and cell-mediated oxidation of LDL. We conclude that enrichment in vivo of macrophages with GSH, significantly decreases cellular oxidative stress, leading to reduced capability of the macrophages to oxidize LDL, and hence GSH may attenuate the development of atherosclerosis.

Analysis of Variance↗
PubMed2002

The biochemistry of aging muscle.

Between the ages of 20 and 80, humans lose approximately 20-30% of their skeletal muscle mass. This age-related loss of muscle mass, sometimes described as 'sarcopenia of old age', is the consequence of complicated multifactorial processes and is commonly associated with osteopenia or osteoporosis. Consequences of the aging changes in muscle are declining physiological function and loss of muscle strength, typically associated with reduced physical activities. Consequently, falls and subsequent serious injuries are prevalent in the elderly. Thus, it is imperative to try and understand the processes, leading to age-related muscle loss, in order to develop means to retard this phenomenon leading to improved quality of life in the elderly. It is possible to divide the causes of muscle aging to intrinsic factors, involving changes at the molecular and cellular levels, and to extrinsic or environmental factors. The purpose of this review is to describe some of the biochemical processes and the possible mechanisms of muscle aging and to evaluate the importance of various extrinsic factors such as nutrition, exercise and limb immobilization. Changes in the aging skeletal muscle are reviewed with regard to: (a) enzyme activities, protein turnover and repair capacities (b) mitochondrial functioning and energy reserve systems (c) ion content and regulation (d) oxidative stress and free radicals (e) nutrition and caloric restriction (f) exercise and limb immobilization.

Aging↗
PubMed2002

Improved development of very-poor-quality human preembryos by coculture with human fallopian ampullary cells.

PURPOSE: To determine whether a confluent culture of fallopian ampullary epithelial cells, taken from women at the end of their reproductive life, is capable of rescuing very-poor-quality preembryos from cleavage arrest and/or degeneration. METHODS: Human preembryos. rejected for transfer or freezing because of very poor quality, and arrested within 24 h of cleavage, were cultured for 5 days in medium alone or over a confluent culture of fallopian ampullary epithelia] cells. Morphological criteria were utilized to assess preembryo degeneration and stage of development. RESULTS: The described coculture rescued preembryos from degeneration, enhancing development to the blastocyst stage 2.2-fold, compared with cultures in medium alone. Furthermore, fully expanded and hatching blastocysts were observed only under coculture conditions. CONCLUSIONS: Very-poor-quality human preembryos may be rescued from degeneration, and their growth and development dramatically improved, when cocultured with a confluent culture of fallopian ampullary epithelial cells.

Cell Communication↗