Novel concepts and nanostructured materials for thermionic-based solar and thermal energy converters.

Thermal and concentrated solar solid-state converters are devices with no moving parts, corresponding to long lifetimes, limited necessity of maintenance, and scalability. Among the solid-state converters, the thermionic-based devices are attracting an increasing interest in the specific growing sector of energy conversion performed at high-temperature. During the last 10 years, hybrid thermionic-based concepts, conceived to cover operating temperatures up to 2000 °C, have been intensively developed. In this review, the thermionic-thermoelectric, photon-enhanced thermionic emission, thermionic-photovoltaic energy converters are extensively discussed. The design and development processes as well as the tailoring of the properties of nanostructured materials performed by the authors are comprehensively described and compared with the advances achieved by the international scientific community.

North Atlantic climate far more predictable than models imply.

Quantifying signals and uncertainties in climate models is essential for the detection, attribution, prediction and projection of climate change1-3. Although inter-model agreement is high for large-scale temperature signals, dynamical changes in atmospheric circulation are very uncertain4. This leads to low confidence in regional projections, especially for precipitation, over the coming decades5,6. The chaotic nature of the climate system7-9 may also mean that signal uncertainties are largely irreducible. However, climate projections are difficult to verify until further observations become available. Here we assess retrospective climate model predictions of the past six decades and show that decadal variations in North Atlantic winter climate are highly predictable, despite a lack of agreement between individual model simulations and the poor predictive ability of raw model outputs. Crucially, current models underestimate the predictable signal (the predictable fraction of the total variability) of the North Atlantic Oscillation (the leading mode of variability in North Atlantic atmospheric circulation) by an order of magnitude. Consequently, compared to perfect models, 100 times as many ensemble members are needed in current models to extract this signal, and its effects on the climate are underestimated relative to other factors. To address these limitations, we implement a two-stage post-processing technique. We first adjust the variance of the ensemble-mean North Atlantic Oscillation forecast to match the observed variance of the predictable signal. We then select and use only the ensemble members with a North Atlantic Oscillation sufficiently close to the variance-adjusted ensemble-mean forecast North Atlantic Oscillation. This approach greatly improves decadal predictions of winter climate for Europe and eastern North America. Predictions of Atlantic multidecadal variability are also improved, suggesting that the North Atlantic Oscillation is not driven solely by Atlantic multidecadal variability. Our results highlight the need to understand why the signal-to-noise ratio is too small in current climate models10, and the extent to which correcting this model error would reduce uncertainties in regional climate change projections on timescales beyond a decade.

Thermoelectric Analysis of ZnSb Thin Films Prepared by ns-Pulsed Laser Deposition.

Zinc antimonide (ZnSb) is a promising thermoelectric material for the temperature range 300­ 600 K. ZnSb thin films were prepared by nanosecond Pulsed Laser Deposition (PLD) to evaluate the performance of nanostructured films for thermoelectric conversion by the determination of the Power Factor. A study of the influence of structural, compositional and thermoelectric properties of thin films is reported as a function of different deposition parameters, such as repetition rate, pulse energy, and substrate temperature. The evaluation of a thin film ZnSb compound with excess Sb has been performed to verify the variation of the thermoelectric properties. The obtained results are reported and discussed in the 300­600 K temperature range.

Risk factors and disease prevalence in 3331 personal check-ups performed in preventive medicine between 2006 and 2011. cross-sectional and follow-up study.

INTRODUCTION: The present data results from a retrospective analysis of 3331 check-ups made in the preventive medicine department of the "ZithaKlinik", named "ZithaGesondheetsZentrum". These check-ups are done for the employee's of several firm's and institutions. According to gender and age, several tests and examinations are performed and the results are given to the person's general practitioner or another doctor of his choice. We will present a global synthesis of all the results but also a follow-up study of persons having performed 2 check-ups or more over a 5-year period. POPULATION: In the cross-sectional part, the analysis is done on 3331 individual check-ups (1447 woman, 1884 men). The average age is 50.3 years +/- 11.4. In the follow-up study, 478 persons (191 women, 287 men) had at least 2 (maximum 5) check-ups in the 5-year period of our observation. Initial age was 54.1 +/- 10.9 years for woman and 51.4 +/- 11.4 for men, respectively 56.4 +/- 10.9 and 53.7+/- 11.2 at their last check-up. RESULTS: An alarming number of persons present with a weight or obesity problem (according to age ranging from 22.0% overweight and 7.3% obese from 18-29 years, respectively 37.5% and 11.3% from 30-49 years, finally 44.0% and 20.6% in the range 50-69 years). Associated risk factors and pathologies (Hypertension, Dyslipidemia, NASH, diabetes type 2 and complete metabolic syndromes) are extremely frequent and getting more so with growing age. Furthermore, physical activity is insufficient in grossly 2/3 of the studied population. The only positive point is a tendency of decreasing tobacco use in all age groups. The follow-up study is frustrating because most of the examined criteria get worse in-between check-ups instead of getting better with changes in lifestyle in an informed population. CONCLUSIONS: Asymptomatic diseases or risk factors for non-communicable diseases are extremely frequent in the population examined. The follow-up data shows that huge parts of this group are not sufficiently conscientious of their problems to act up and change their life-style or seek adapted pharmacological prevention. Absolute number of risk factors (prevalence) or pathologies rise evidently with age but incidence (newly discovered pathologies after a first, second or a record of 21 check-ups with our services) rises less. Life-style changes are rare or insufficient to change the pathological value back to normal or therapeutically range. Even with several biases (retrospective design, selection bias, ...) our study puts similar problems forward in the population as ORISCAV. The astonishing (better than national records) results in tobacco use is probably due to a selection of more health-oriented patients and of a higher socio-educative-economic level. Alcohol abuse was very low but probably due to inadequate screening methods. A better health promotion advocating healthier living must be associated with better communication and new motivational tools. Therapeutical education for patients with chronic non-communicable diseases will be the challenge of the near future as their prevalences increase due to ageing of the population and worse individual lifestyles. In this task, efforts must be made on the personal level (health-team with the individual patient) but also on the national level (legal frame work for patient education by multi-professional teams as they exist already in neighbour states).

Differential activation of mitogen-activated protein kinase signalling pathways in the hippocampus of CRND8 transgenic mouse, a model of Alzheimer's disease.

Transgenic Centre for Research in Neurodegenerative Diseases 8 (TgCRND8) mice expressing a double mutant form of human amyloid precursor protein represent a good model of Alzheimer's disease, and can be useful to clarify the involvement of mitogen-activated protein kinases (MAPK) dysregulation in the pathophysiology of this neurodegenerative disorder. Activation of extracellular regulated kinase (ERK) 1/2, jun kinase (JNK) and p38MAPK was studied in the hippocampus of 7-month-old TgCRND8 mice by immunohistochemistry and Western blot analysis using antibodies selective for the phosphorylated, and thus active, forms of the enzymes. We demonstrated that the three main MAPK pathways were differentially activated in cells of the hippocampus of TgCRND8 mice in comparison to wild type (Wt) littermates, p38MAPK and JNK being more activated, while ERK less activated. p38MAPK was significantly activated in microglia, astrocytes and neurons, around and distant from the plaques. JNK was highly activated in cells closely surrounding the plaques. No difference was observed in the activation of the two major bands of JNK, at a molecular weight of 46 kDa and 54 kDa. These data indicate the possible involvement of p38MAPK and JNK pathways dysregulation in the pathogenesis of Alzheimer's disease. The ERK2 isoform of the ERK pathway was less activated in the hippocampal dentate gyrus of Tg mice in basal conditions. Furthermore activation of the ERK pathway by ex vivo cholinergic stimulation with carbachol caused significantly higher activation of ERK in the hippocampus of Wt mice than in Tg mice. These findings may pose a molecular basis for the memory disruption of Alzheimer's disease, since proper functioning of the basal forebrain cholinergic neurons and of ERK2 is critical for memory formation.

Endocrine disorders in pediatric - onset Langerhans Cell Histiocytosis.

Langerhans Cell Histiocytosis (LCH) is a rare disorder with a great variety of clinical manifestations. The purpose of this retrospective study was to evaluate the pattern and the long-term course of clinical, laboratorial and radiological findings in pediatric-onset LCH. We reviewed 46 children with histological diagnosis of LCH. Ten children (22%) showed endocrine disorders. Central diabetes insipidus (DI) was observed in all ten patients; GH deficiency was confirmed in four and hypogonadism in two children. There were no adrenal, prolactin or thyroid axis abnormalities. Obesity was observed in three patients. Eight patients showed soft tissue infiltration and five bone involvement. The MRI showed a lack of posterior pituitary bright spot in all DI patients; infundibular infiltration (II) associated or not with sellar or supra-sellar mass was observed in 4 patients. We conclude that the investigation of LCH, a multi-systemic disease, should include central nervous system images. The presence of II and/or DI should raise the diagnosis of LCH. Complete endocrine evaluation, allowing an early hormone therapy, is required to obtain a better quality of life in children with LCH.

Charon's size and an upper limit on its atmosphere from a stellar occultation.

Pluto and its satellite, Charon (discovered in 1978; ref. 1), appear to form a double planet, rather than a hierarchical planet/satellite couple. Charon is about half Pluto's size and about one-eighth its mass. The precise radii of Pluto and Charon have remained uncertain, leading to large uncertainties on their densities. Although stellar occultations by Charon are in principle a powerful way of measuring its size, they are rare, as the satellite subtends less than 0.3 microradians (0.06 arcsec) on the sky. One occultation (in 1980) yielded a lower limit of 600 km for the satellite's radius, which was later refined to 601.5 km (ref. 4). Here we report observations from a multi-station stellar occultation by Charon, which we use to derive a radius, R(C) = 603.6 +/- 1.4 km (1sigma), and a density of rho = 1.71 +/- 0.08 g cm(-3). This occultation also provides upper limits of 110 and 15 (3sigma) nanobar for an atmosphere around Charon, assuming respectively a pure nitrogen or pure methane atmosphere.

Comparison between flurbiprofen and its nitric oxide-releasing derivatives HCT-1026 and NCX-2216 on Abeta(1-42)-induced brain inflammation and neuronal damage in the rat.

Brain inflammation is an underlying factor in the pathogenesis of Alzheimers disease (AD). We investigated, in vivo, whether differences exist in the anti-inflammatory and neuroprotective actions of flurbiprofen and its two nitric oxide-donor derivatives, HCT-1026 and NCX-2216, and the ability of these two derivatives to release nitric oxide in the brain. In adult rats injected into the nucleus basalis with preaggregated Abeta(1-42) we investigated glia reaction, the induction of inducible nitric oxide synthase (iNOS), the activation of p38 mitogen-activated protein kinase (p38MAPK) pathway and the number of choline acetyltransferase (ChAT)-positive neurons and, in naive rats we investigated, by microdialysis, cortical extracellular levels of nitrite. Injection of Abeta(1-42) induced iNOS and activation of p38MAPK 7 days after injection and an intense microglia and astrocyte reaction along with a marked reduction in the number ChAT-positive neurons, persisting up to at least 21 days. Flurbiprofen, HCT-1026 and NCX-2216 (15 mg/kg) significantly attenuated the Abeta(1-42)-induced glia reaction, iNOS induction and p38MAPK activation 7 days after treatment and astrocytes reaction 21 days after treatment. On an equimolar basis, HCT-1026 resulted the most active agent in reducing the Abeta(1-42)-induced microglia reaction. The cholinergic cell loss was also significantly reduced by 21 days of HCT-1026 treatment. No differences in body weight were found between the animals treated for 21 days with 15 mg/kg of either HCT-1026 or NCX-2216 and the controls. Oral administration of HCT-1026 (15 mg/kg) or NCX-2216 (100 mg/kg) to naive rats was followed by significant and long lasting increases in cortical nitrite levels. These findings indicate that the addition of a nitric oxide donor potentiates the anti-inflammatory activity of flurbiprofen in a model of brain inflammation.

Midarm computerized tomography fat, muscle and total areas correlation with nutritional assessment data.

BACKGROUND AND OBJECTIVES: Correlated nutritional assessment data (anthropometric, bioimpedance and biochemical) with computerized tomography (CT) of total, muscle and fat midarm areas. Total body fat and fat-free mass were estimated using bioimpedance. Daily urinary urea and creatinine were also quantified. In all, 28 subjects (13 males, 15 females) were evaluated and, they were clinically divided in obese, malnourished and control subjects. DESIGN: Quantification of total, fat muscle midarm areas by tomography and anthropometry and total body fat and free-fat mass by bioimpedance. RESULTS: CT values were 29% higher for fat area and 4-5% lower for total and muscle midarm areas compared against anthropometric data. The midarm skinfold thickness highly correlated with CT fat midarm area. Total body fat and free-fat mass bioimpedance data showed significant correlation with CT midarm data. Urinary creatinine correlated with CT muscle midarm area. CONCLUSION: Utilization of anthropometry can lead to error estimation of fat and fat-free arm areas and that bioimpedance gives fair correlation between total body and CT midarm measurements.

Experimental brain inflammation and neurodegeneration as model of Alzheimer's disease: protective effects of selective COX-2 inhibitors.

Epidemiological studies indicate that long-term treatment with non-steroidal anti-inflammatory drugs reduces the risk of Alzheimer Disease and may delay its onset or slow its progression. Neuroinflammation occurs in vulnerable regions of the Alzheimer's disease (AD) brain where highly insoluble beta-amyloid (Abeta) peptide deposits and neurofibrillary tangles, as well as damaged neurons and neurites, provide stimuli for inflammation. To elucidate the complex role of inflammation in neurodegenerative processes and the efficacy of selective COX-2 inhibitors in AD, we examined whether the attenuation of brain inflammatory reaction by selective COX-2 inhibitors may protect neurons against neurodegeneration. The data reported in this review show that in in vivo models of brain inflammation and neurodegeneration, the administration of selective COX-2 inhibitors prevent not only the inflammatory reaction, but also the cholinergic hypofunction. Our data may help elucidate the epidemiological findings indicating that anti-inflammatory agents, in particular NSAIDs, reduce the risk of developing AD and may slow its progression.

The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo.

Brain inflammatory processes underlie the pathogenesis of Alzheimer's disease, and non-steroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this work was to study in vivo whether attenuation of brain inflammatory response to excitotoxic insult by the selective cyclooxygenase-2 inhibitor, rofecoxib, may prevent neurodegeneration, as a contribution to a better understanding of the role inflammation plays in the pathology of Alzheimer's disease. We investigated, by immunohistochemical methods, glia reaction, the activation of p38 mitogen-activated protein kinase (p38MAPK) pathway with an antibody selective for the phosphorylated form of the enzyme and the number of choline acetyltransferase-positive neurons and, by in vivo microdialysis, cortical extracellular levels of acetylcholine following the injection of quisqualic acid into the right nucleus basalis of adult rats. Seven days after injection, a marked reduction in the number of choline acetyltransferase-positive neurons was found, along with an intense glia reaction, selective activation of p38MAPK at the injection site and a significant decrease in the extracellular levels of acetylcholine in the cortex ipsilateral to the injection site. The loss of cholinergic neurons persisted for at least up to 28 days. Rofecoxib (3 mg/kg/day, starting 1 h prior to injection of quisqualic acid) treatment for 7 days significantly attenuated glia activation and prevented the loss of choline acetyltransferase-positive cells and a decrease in cortical acetylcholine release. The prevention of cholinergic cell loss by rofecoxib occurred concomitantly with the inhibition of p38MAPK phosphorylation. Our findings suggest an important role of brain inflammatory reaction in cholinergic degeneration and demonstrate a neuroprotective effect of rofecoxib, presumably mediated through the inhibition of p38MAPK phosphorylation.

Effect of subchronic administration of metrifonate, rivastigmine and donepezil on brain acetylcholine in aged F344 rats.

The changes in extracellular acetylcholine levels were investigated by microdialysis in the cortex and hippocampus of aging rats after administration of metrifonate (80 mg/kg), rivastigmine (0.75 mg/kg), donepezil (1.5 mg/kg) or vehicle for 21 days (twice daily p.o.). Eighteen h after the last administration, cholinesterase inhibition was 85, 52 and 39% after metrifonate, rivastigmine and donepezil, respectively, and was accompanied by 988, 590 and 75% increase in cortical acetylcholine level. In the hippocampus, metrifonate and rivastigmine brought about a 169 and 108% increase in acetylcholine levels. A challenge dose of metrifonate, rivastigmine and donepezil was followed by a further increase in cortical and hippocampal acetylcholine levels. The retrograde perfusion of the M(2)-M(4) receptor antagonist AFDX-384 (10 microM) induced a 500 and 300% increase in cortical and hippocampal acetylcholine release, in control and rivastigmine-treated rats, respectively, no increase in metrifonate-treated rats, and a 210% increase in donepezil-treated rats. In conclusion, chronic treatment of aging rats with metrifonate, rivastigmine and donepezil induces a long-lasting increase in acetylcholine levels, and reveals marked differences between the three drugs.

Normal pituitary hypertrophy as a frequent cause of pituitary incidentaloma: a follow-up study.

Enlargement of the pituitary gland is a frequent cause of incidentaloma and of referrals to endocrinologists for hormonal evaluation and therapeutic advice. In neuroradiological series, 25-50% of healthy women who are 18-35 yr old have a convex superior pituitary contour, but pituitary height exceeds 9 mm in less than 0.5% of cases. This study was performed to provide thorough clinical and hormonal data and long-term endocrinological and imaging follow-up data on subjects with incidentally discovered pituitary hypertrophy (height > 9 mm). Seven eugonadal nulliparous women, 15-27 yr old, referred between 1989 and 1998 with incidentally diagnosed pituitary gland enlargement (height > 9 mm) and a suspected pituitary tumor, were studied. At presentation and at yearly intervals, PRL plasma levels and corticotropic, somatotropic, and thyrotropic pituitary function were measured; and pituitary dimensions and signal on magnetic resonance imaging (MRI), before and after iv gadolinium-diethylene-triamine-pentaacetic acid injection, were assessed. PRL plasma levels were normal; and corticotropic, somatotropic, and thyrotropic pituitary function was considered normal in all cases. In all the women, the upper boundary of the pituitary was convex, on MRI, and touched the optic chiasm in four cases. The width and anteroposterior diameter of the gland were normal. The pituitary itself seemed normal, with a homogeneous signal, on plain and dynamic studies with iv contrast injection. Despite normal initial hormone values, two women underwent surgery, by the transsphenoidal approach, in another center. During surgery, the pituitary seemed normal in both cases, with no evidence of tumoral or inflammatory processes. Biopsy specimens showed the morphologic characteristics of a normal, nonhyperplastic pituitary gland. All seven women were seen at yearly intervals for 2-8 yr (median, 4 yr). Clinical and hormonal status remained stable, as did the structure and size of pituitary, on serial MRI. No tumor formation occurred, supporting the diagnosis of physiologic hypertrophy of the pituitary gland. In conclusion, these observations suggest that careful examination of MRI results may help to distinguish physiologic pituitary hypertrophy from pituitary tumors and infiltrating lesions. The former diagnosis is confirmed by normal baseline pituitary function in extensive hormonal tests. Correct identification of such patients is important to avoid unnecessary pituitary surgery and costly MRI surveillance.

Autonomic nervous system activity imbalance in cardiomyopathic hamster.

There is strong evidence that autonomic imbalance plays an important role in progression of heart failure. Analysis of heart rate variability (HRV) has achieved substantial acceptance as a noninvasive method for the assessment of autonomic tone. The purpose of this investigation was to study HRV in an experimental model of heart failure using cardiomyopathic (BIO TO.2) hamsters. Animals showed an autonomic imbalance of cardiac control that seems due to attenuation of parasympathetic activity and an enhanced sympathetic tone. The reduction of parasympathetic activity in BIO TO.2 hamsters is suggested by (a) the reduction of the high-frequency (HF) spectrum, and (b) the lack of atropine to generate a response. The increased sympathetic activity is indicated by (a) the decreased time-domain indexes, (b) the increased LF/HF ratio of the power spectrum, and (c) the alteration of HRV indexes induced by propranolol. These results support the notion that in heart failure, there is a similar autonomic imbalance in both human and hamster and suggest that the cardiomyopathic hamster is a suitable experimental model for studying the involvement of the autonomic nervous system in the progression of heart failure.

The impact of co-morbid risk factors at the start of dialysis upon the survival of ESRD patients.

By using a computerized database, we have catalogued the presence of 29 co-morbid risk factors in 683 patients with end-stage renal disease who started dialysis from 1970 through 1989, with follow-up through 1992. The authors hypothesized that current end-stage renal disease patients have more serious co-morbid risk factors impacting upon their mortality rate. Quantitation of dialysis patient co-morbidity, as a measure of patient illness, is lacking in the general nephrology literature. Seven co-morbid risk factors have been reserved for new dialysis patients: hypertension, low albumin, cerebral vascular disease, peripheral vascular disease, pre-existing cardiac disease, abnormal EKG/old myocardial infarction, and congestive heart failure. Except for low serum albumin, the proportion of patients with the six other co-morbid risk factors has increased significantly over this 20-year period (p < 0.0001, chi-square test for hypertension, peripheral vascular disease, pre-existing cardiac disease, abnormal EKG/old myocardial infarction, and congestive heart failure, and p < 0.006 for cerebral vascular disease). In addition, the co-morbid risk factors of hypertension, low serum albumin, and pre-existing cardiac disease at the start of dialysis were strongly prognostic of survival. The Cox proportional hazards regression model identified these three risks, among other factors, that were significantly associated with a decreased survival, with risk ratios ranging from 1.40-1.66. These results support the authors' hypothesis that incoming end-stage renal disease patients, who recently start dialysis, are sicker than in the earlier years of the authors' program. If the authors' patients reflect the national end-stage renal disease population, the presence of co-morbid risk factors may, in part, explain the continuing high mortality of dialysis patients.

Comparison of methods for measuring albumin in peritoneal dialysis and hemodialysis patients.

Serum albumin levels have been used extensively as an indicator of morbidity in patients with end-stage renal disease. Recent evidence suggests that albumin levels vary considerably in hemodialysis patients depending on the laboratory method used, but formulas for comparing albumin values by different methods have not been developed. We prospectively evaluated the effects of measuring albumin by three different methods on paired plasma and serum from 23 patients on continuous ambulatory peritoneal dialysis (CAPD) and 53 patients on chronic maintenance hemodialysis. Plasma and serum gave virtually identical results independent of method used. In CAPD patients, bromcresol green and nephelometry gave nearly identical albumin measurements through the entire range of plasma levels. In contrast, bromcresol purple gave values that were 9.9 percent +/- 1.3 percent lower (P < 0.05). Hemodialysis patients showed a similar pattern with close agreement between bromcresol green and nephelometry, but bromcresol purple gave lower albumin levels by 19.1 percent +/- 1.2 percent (P < 0.05). The discrepancy in albumin in CAPD patients was significantly less than in the hemodialysis patients (P < 0.05), suggesting that there were fewer interfering substances in the blood of CAPD patients than in hemodialysis patients. Linear regression analysis was used to develop simple formulas for comparing albumin values obtained by the different methods in CAPD and hemodialysis patients. These studies show that values for albumin in blood vary significantly by method of analysis in CAPD and hemodialysis patients. By the use of these formulas, it becomes possible to compare albumin values between centers using different methods for the purpose of quality management.

Home hemodialysis: patient outcomes during a 24-year period of time from 1970 through 1993.

In the United States, from 1983 to 1993, home hemodialysis use has decreased from 6% to 1.3% of the dialysis population, whereas continuous ambulatory peritoneal dialysis (CAPD) has increased to 20%. Most home hemodialysis programs have withered away because of current patient mix, increase in CAPD, proliferation of outpatient centers, disinterest in nephrologists, and fear of self-cannulation by patients. From 1970 through 1993, 896 patients began dialysis at North Shore and were followed up through 1994. During this period, 687 patients were on in-center hemodialysis, 95 on CAPD, 74 on home hemodialysis, and 40 on in-center peritoneal dialysis. The home hemodialysis patients were younger, with a median age of 44 versus 59 years for in-center hemodialysis patients, and had less comorbidity. The home hemodialysis group had fewer diabetic patients and no renal vascular patients. The 5-year and median survival estimates were significantly better for the home hemodialysis patients versus other dialysis modalities. More home hemodialysis patients received transplants. Compared with the other dialysis modalities, home hemodialysis patients showed significantly improved survival rates. When matched by age, sex, and end-stage renal disease (ESRD) diagnosis to corresponding in-center hemodialysis, the home hemodialysis patients still had significantly better survival rates, but the home hemodialysis patients had less comorbidity. In conclusion, home hemodialysis patients survive longer and have better rehabilitation than other dialysis patients. Reasons for better survival in addition to a younger age and more favorable ESRD diagnosis may include less comorbidity, more patient involvement, and longer dialysis time. Because of these better outcomes, home hemodialysis should be offered to more ESRD patients.