Showing papers by "University of Alabama at Birmingham published in 2001"
TL;DR: Genetic evidence is presented that different mutations of the human gene FOXP3, the ortholog of the gene mutated in scurfy mice (Foxp3), causes IPEX syndrome.
Abstract: IPEX is a fatal disorder characterized by immune dysregulation, polyendocrinopathy, enteropathy and X-linked inheritance (MIM 304930). We present genetic evidence that different mutations of the human gene FOXP3, the ortholog of the gene mutated in scurfy mice (Foxp3), causes IPEX syndrome. Recent linkage analysis studies mapped the gene mutated in IPEX to an interval of 17-20-cM at Xp11. 23-Xq13.3.
3,224 citations
TL;DR: GSK3beta has a central role regulating neuronal plasticity, gene expression, and cell survival, and may be a key component of certain psychiatric and neurodegenerative diseases.
1,447 citations
TL;DR: The functional role of astrocytes as immune effector cells and how this may influence aspects of inflammation and immune reactivity within the brain follows, emphasizing the involvement of astracytes in promoting Th2 responses.
Abstract: Astrocytes are the major glial cell within the central nervous system (CNS) and have a number of important physiological properties related to CNS homeostasis. The aspect of astrocyte biology addressed in this review article is the astrocyte as an immunocompetent cell within the brain. The capacity of astrocytes to express class II major histocompatibility complex (MHC) antigens and costimulatory molecules (B7 and CD40) that are critical for antigen presentation and T-cell activation are discussed. The functional role of astrocytes as immune effector cells and how this may influence aspects of inflammation and immune reactivity within the brain follows, emphasizing the involvement of astrocytes in promoting Th2 responses. The ability of astrocytes to produce a wide array of chemokines and cytokines is discussed, with an emphasis on the immunological properties of these mediators. The significance of astrocytic antigen presentation and chemokine/cytokine production to neurological diseases with an immunological component is described.
1,220 citations
TL;DR: Threshold values for sperm concentration, motility, and morphology can be used to classify men as subfertile, of indeterminate fertility, or fertile and none of the measures are diagnostic of infertility.
Abstract: Background Although semen analysis is routinely used to evaluate the male partner in infertile couples, sperm measurements that discriminate between fertile and infertile men are not well defined. Methods We evaluated two semen specimens from each of the male partners in 765 infertile couples and 696 fertile couples at nine sites. The female partners in the infertile couples had normal results on fertility evaluation. The sperm concentration and motility were determined at the sites; semen smears were stained at the sites and shipped to a central laboratory for an assessment of morphologic features of sperm with the use of strict criteria. We used classification-and-regression-tree analysis to estimate threshold values for subfertility and fertility with respect to the sperm concentration, motility, and morphology. We also used an analysis of receiver-operating-characteristic curves to assess the relative value of these sperm measurements in discriminating between fertile and infertile men. Results The su...
1,129 citations
TL;DR: This review provides a contemporary interpretation of the biological properties, function, epidemiology, and treatment of HSV diseases.
1,119 citations
TL;DR: Splenic MZ and B1 B cells endowed with a "natural memory" provide a bridge between the very early innate and the later appearing adaptive immune response.
978 citations
TL;DR: Both age of L2 learning and amount of continued L1 use were found to affect degree of foreign accent, and gender, length of residence in an L2-speaking country and self-estimated L1 ability, on the other hand, were not found to have a significant, independent effect on overall L2 pronunciation accuracy.
892 citations
TL;DR: Hypertension and diabetes mellitus were positively associated with cognitive decline over 6 years in this late middle-aged population and interventions aimed at hypertension or diabetes that begin before age 60 might lessen the burden of cognitive impairment in later life.
Abstract: Objective: To perform serial neuropsychological assessments to detect vascular risk factors for cognitive decline in the Atherosclerosis Risk in Communities cohort, a large biracial, multisite, longitudinal investigation of initially middle-aged individuals. Methods: The authors administered cognitive assessments to 10,963 individuals (8,729 white individuals and 2,234 black individuals) on two occasions separated by 6 years. Subjects ranged in age at the first assessment from 47 to 70 years. The cognitive assessments included the delayed word recall (DWR) test, a 10-word delayed free recall task in which the learning phase included sentence generation with the study words, the digit symbol subtest (DSS) of the Wechsler Adult Intelligence Scale–Revised and the first-letter word fluency (WF) test using letters F, A, and S. Results: In multivariate analyses (controlling for demographic factors), the presence of diabetes at baseline was associated with greater decline in scores on both the DSS and WF (p Conclusions: Hypertension and diabetes mellitus were positively associated with cognitive decline over 6 years in this late middle-aged population. Interventions aimed at hypertension or diabetes that begin before age 60 might lessen the burden of cognitive impairment in later life.
855 citations
TL;DR: It is shown that CHIP functions with Hsc70 to sense the folded state of CFTR and targets aberrant forms for proteasomal degradation by promoting their ubiquitination.
Abstract: The folding of both wild-type and mutant forms of the cystic-fibrosis transmembrane-conductance regulator (CFTR), a plasma-membrane chloride-ion channel, is inefficient. Most nascent CFTR is retained in the endoplasmic reticulum and degraded by the ubiquitin proteasome pathway. Aberrant folding and defective trafficking of CFTRDeltaF508 is the principal cause of cystic fibrosis, but how the endoplasmic-reticulum quality-control system targets CFTR for degradation remains unknown. CHIP is a cytosolic U-box protein that interacts with Hsc70 through a set of tetratricorepeat motifs. The U-box represents a modified form of the ring-finger motif that is found in ubiquitin ligases and that defines the E4 family of polyubiquitination factors. Here we show that CHIP functions with Hsc70 to sense the folded state of CFTR and targets aberrant forms for proteasomal degradation by promoting their ubiquitination. The U-box appeared essential for this process because overexpresion of CHIPDeltaU-box inhibited the action of endogenous CHIP and blocked CFTR ubiquitination and degradation. CHIP is a co-chaperone that converts Hsc70 from a protein-folding machine into a degradation factor that functions in endoplasmic-reticulum quality control.
850 citations
TL;DR: In the analysis of the genome, a large number of new uncharacterized genes predicted to encode proteins that either reside on the surface of the cell or are secreted are identified and there may be new targets for vaccine and antibiotic development.
Abstract: Streptococcus pneumoniae is among the most significant causes of bacterial disease in humans. Here we report the 2,038,615-bp genomic sequence of the gram-positive bacterium S. pneumoniae R6. Because the R6 strain is avirulent and, more importantly, because it is readily transformed with DNA from homologous species and many heterologous species, it is the principal platform for investigation of the biology of this important pathogen. It is also used as a primary vehicle for genomics-based development of antibiotics for gram-positive bacteria. In our analysis of the genome, we identified a large number of new uncharacterized genes predicted to encode proteins that either reside on the surface of the cell or are secreted. Among those proteins there may be new targets for vaccine and antibiotic development.
809 citations
TL;DR: A role for IL-6 and its soluble receptor (sIL-6R) in controlling this pattern of leukocyte recruitment during peritoneal inflammation is presented and supports transition between the early predominantly neutrophilic stage of an infection and the more sustained mononuclear cell influx.
TL;DR: The results suggest that BLyS may be a useful marker for early activation of an autoimmune diathesis and likely plays a critical role in triggering activation of self-Ag-driven autoimmune B cells in human SLE and may provide an effective therapeutic target in systemic autoimmunity.
Abstract: Increased levels of B lymphocyte stimulator (BLyS) are associated with systemic autoimmunity in animal models of spontaneous autoimmune disease, and transgenic animals expressing BLyS develop typical autoimmune disease. Here, we demonstrate significant elevations of BLyS in the patients with systemic lupus erythematosus (SLE). The BLyS isolated from the sera of SLE patients had the same m.w. as the natural soluble form and was able to stimulate B cell activation in vitro. Increased BLyS in SLE patients was partially associated with higher levels of anti-dsDNA Ab of the IgG, IgM, and IgA classes, but not associated with the disease activity. Our results suggest that BLyS may be a useful marker for early activation of an autoimmune diathesis and likely plays a critical role in triggering activation of self-Ag-driven autoimmune B cells in human SLE. BLyS may provide an effective therapeutic target in systemic autoimmunity.
TL;DR: Reactive oxygen species may alter endothelium-dependent vascular relaxation not only by the interaction of O2·− with NO· but also through interactions between peroxynitrite and tetrahydrobiopterin.
Abstract: Background—Altered endothelial cell nitric oxide (NO·) production in atherosclerosis may be due to a reduction of intracellular tetrahydrobiopterin, which is a critical cofactor for NO synthase (NOS). In addition, previous literature suggests that inactivation of NO· by increased vascular production superoxide (O2·−) also reduces NO· bioactivity in several disease states. We sought to determine whether these 2 seemingly disparate mechanisms were related. Methods and Results—Endothelium-dependent vasodilation was abnormal in aortas of apoE-deficient (apoE−/−) mice, whereas vascular superoxide production (assessed by 5 μmol/L lucigenin) was markedly increased. Treatment with either liposome-entrapped superoxide dismutase or sepiapterin, a precursor to tetrahydrobiopterin, improved endothelium-dependent vasodilation in aortas from apoE−/− mice. Hydrogen peroxide had no effect on the decay of tetrahydrobiopterin, as monitored spectrophotometrically. In contrast, superoxide modestly and peroxynitrite strikingl...
TL;DR: These studies demonstrate that in contrast to protein-free enterobacterial LPS, a similarly purified preparation of P. gingivalis LPS exhibited potent Toll-like receptor 2 (TLR2), rather than TLR4, agonist activity to elicit gene expression and cytokine secretion in murine macrophages and transfectants.
Abstract: Lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis has been reported to differ structurally and functionally from enterobacterial LPS. These studies demonstrate that in contrast to protein-free enterobacterial LPS, a similarly purified preparation of P. gingivalis LPS exhibited potent Toll-like receptor 2 (TLR2), rather than TLR4, agonist activity to elicit gene expression and cytokine secretion in murine macrophages and transfectants. More importantly, TLR2 stimulation by this P. gingivalis LPS preparation resulted in differential expression of a panel of genes that are normally induced in murine macrophages by Escherichia coli LPS. These data suggest that (i) P. gingivalis LPS does not signal through TLR4 and (ii) signaling through TLR2 and through TLR4 differs quantitatively and qualitatively. Our data support the hypothesis that the shared signaling pathways elicited by TLR2 and by TLR4 agonists must diverge in order to account for the distinct patterns of inflammatory gene expression.
TL;DR: Oseltamivir treatment did not affect the influenza-specific antibody response and is an efficacious and well-tolerated therapy for influenza in children when given within 48 h of onset of illness.
Abstract: Background.Oral oseltamivir administration is effective treatment for influenza in adults. This study was conducted to determine the efficacy, safety and tolerability of oseltamivir in children with influenza.Methods.In this randomized, double blind, placebo-controlled study, children 1 through 12 y
TL;DR: It is shown that malignant human ovarian epithelial tumor cells express very high levels of stromal-derived factor-1, which induces DC2 precursor (preDC2) chemotaxis and adhesion/transmigration, upregulates preDC2 very late antigen (VLA)-5, and protects preDC1s from tumor macrophage interleukin-10–induced apoptosis, all through CXC chemokine receptor-4.
Abstract: Dendritic-cell (DC) trafficking and function in tumors is poorly characterized, with studies confined to myeloid DCs (DC1s). Tumors inhibit DC1 migration and function, likely hindering specific immunity. The role of plasmacytoid DCs (DC2s) in tumor immunity is unknown. We show here that malignant human ovarian epithelial tumor cells express very high levels of stromal-derived factor-1, which induces DC2 precursor (preDC2) chemotaxis and adhesion/transmigration, upregulates preDC2 very late antigen (VLA)-5, and protects preDC2s from tumor macrophage interleukin-10-induced apoptosis, all through CXC chemokine receptor-4. The VLA-5 ligand vascular-cell adhesion molecule-1 mediated preDC2 adhesion/transmigration. Tumor preDC2s induced significant T-cell interleukin-10 unrelated to preDC2 differentiation or activation state, and this contributed to poor T-cell activation. Myeloid precursor DCs (preDC1s) were not detected. Tumors may weaken immunity by attracting preDC2s and protecting them from the harsh microenvironment, and by altering preDC1 distribution.
TL;DR: The findings demonstrate a consistent pattern of health risk behaviors and adverse biological outcomes associated with less perceived parental monitoring and additional research needs to focus on developing theoretical models that help explain the influence of familial environment on adolescent health.
Abstract: Context. Contemporary threats to adolescents9 health are primarily the consequence of risk behaviors and their related adverse outcomes. Identifying factors associated with adolescents9 risk behaviors is critical for developing effective prevention strategies. A number of risk factors have been identified, including familial environment; however, few studies have examined the impact of parental monitoring. Objective. To examine the influence of less perceived parental monitoring on a spectrum of adolescent health-compromising behaviors and outcomes. Design. Survey. Setting. A family medicine clinic. Participants. To assess eligibility, recruiters screened a sample of 1130 teens residing in low-income neighborhoods. Adolescents were eligible if they were black females, between the ages of 14 and 18 years, sexually active in the previous 6 months, and provided written informed consent. Most teens (n = 609) were eligible, with 522 (85.7%) agreeing to participate. Main Outcome Measures. Variables in 6 domains were assessed, including: sexually transmitted diseases, sexual behaviors, marijuana use, alcohol use, antisocial behavior, and violence. Results. In logistic regression analyses, controlling for observed covariates, adolescents perceiving less parental monitoring were more likely to test positive for a sexually transmitted disease (odds ratio [OR]: 1.7), report not using a condom at last sexual intercourse (OR: 1.7), have multiple sexual partners in the past 6 months (OR: 2.0), have risky sex partners (OR: 1.5), have a new sex partner in the past 30 days (OR: 3.0), and not use any contraception during the last sexual intercourse episode (OR: 1.9). Furthermore, adolescents perceiving less parental monitoring were more likely to have a history of marijuana use and use marijuana more often in the past 30 days (OR: 2.3 and OR: 2.5, respectively); a history of alcohol use and greater alcohol consumption in the past 30 days (OR: 1.4 and OR: 1.9, respectively); have a history of arrest (OR: 2.1); and there was a trend toward having engaged in fights in the past 6 months (OR: 1.4). Conclusions. The findings demonstrate a consistent pattern of health risk behaviors and adverse biological outcomes associated with less perceived parental monitoring. Additional research needs to focus on developing theoretical models that help explain the influence of familial environment on adolescent health and develop and evaluate interventions to promote the health of adolescents.
TL;DR: Serum specimens from 46 women with preconceptional immunity against CMV that were obtained during the previous pregnancy and the current pregnancy were analyzed for antibodies against the strain-specific epitopes of CMV glycoprotein H.
Abstract: Background Preconceptional immunity against cytomegalovirus (CMV) provides only partial protection against intrauterine transmission of the virus. Whether congenital CMV infection in the offspring of women who are seropositive for CMV can occur after maternal reinfection with a different strain of CMV is unknown. Methods Serum specimens from 46 women with preconceptional immunity against CMV that were obtained during the previous pregnancy and the current pregnancy were analyzed for antibodies against the strain-specific epitopes of CMV glycoprotein H. Virus-neutralizing activity in maternal serum samples was measured against the AD169 laboratory strain of CMV and the CMV isolates available from seven infected infants. In addition, the nucleotide sequences of the glycoprotein H gene from the seven CMV isolates were determined. Results Eleven of the 16 mothers with infected infants (69 percent) had antibodies against the glycoprotein H epitopes present on two laboratory strains of CMV, AD169 and Towne. Ten...
TL;DR: It is essential to consider not only the action of IL‐6 itself, but also the effect sIL‐6R may have on cellular processes when thinking about the inflammatory capability of IL-6.
Abstract: Interleukin 6 (IL-6) performs a prominent role during disease and has been described as both a pro- and anti-inflammatory cytokine. A key feature in the regulation of IL-6 responses has been the identification of a soluble interleukin 6 receptor (sIL-6R), which forms a ligand-receptor complex with IL-6 that is capable of stimulating a variety of cellular responses including proliferation, differentiation and activation of inflammatory processes. Elevated sIL-6R levels have been documented in numerous clinical conditions indicating that its production is coordinated as part of a disease response. Thus, sIL-6R has the potential to regulate both local and systemic IL-6-mediated events. This review will outline the central role of sIL-6R in the coordination of IL-6 responses. Details relating to the mechanisms of sIL-6R production will be provided, while the potential significance of sIL-6R during the development of clinical conditions will be emphasized. We want to convey, therefore, that when thinking about the inflammatory capability of IL-6, it is essential to consider not only the action of IL-6 itself, but also the effect sIL-6R may have on cellular processes.
TL;DR: Sequence analysis of DNA samples from patients representing different Alexander disease phenotypes revealed that most cases are associated with non-conservative mutations in the coding region of GFAP, the first example of a primary genetic disorder of astrocytes, one of the major cell types in the vertebrate CNS.
Abstract: Alexander disease is a rare disorder of the central nervous system of unknown etiology. Infants with Alexander disease develop a leukoencephalopathy with macrocephaly, seizures and psychomotor retardation, leading to death usually within the first decade; patients with juvenile or adult forms typically experience ataxia, bulbar signs and spasticity, and a more slowly progressive course. The pathological hallmark of all forms of Alexander disease is the presence of Rosenthal fibers, cytoplasmic inclusions in astrocytes that contain the intermediate filament protein GFAP in association with small heat-shock proteins. We previously found that overexpression of human GFAP in astrocytes of transgenic mice is fatal and accompanied by the presence of inclusion bodies indistinguishable from human Rosenthal fibers. These results suggested that a primary alteration in GFAP may be responsible for Alexander disease. Sequence analysis of DNA samples from patients representing different Alexander disease phenotypes revealed that most cases are associated with non-conservative mutations in the coding region of GFAP. Alexander disease therefore represents the first example of a primary genetic disorder of astrocytes, one of the major cell types in the vertebrate CNS.
TL;DR: It was found that lacZ expression was primarily limited to the central nervous system, but therein was widespread in neurons and ependyma, suggesting that the hGFAP promoter is active in a multi‐potential neural stem cell.
Abstract: With the goal of performing astrocyte-specific modification of genes in the mouse, we have generated a transgenic line expressing Cre recombinase under the control of the human glial fibrillary acidic protein (hGFAP) promoter Activity was monitored by crossing the hGFAP-cre transgenics with either of two reporter lines carrying a lacZ gene whose expression requires excision of loxP-flanked stop sequences We found that lacZ expression was primarily limited to the central nervous system, but therein was widespread in neurons and ependyma Cell types within the brain that notably failed to activate lacZ expression included Purkinje neurons of the cerebellum and choroid plexus epithelium Onset of Cre expression began in the forebrain by e135, suggesting that the hGFAP promoter is active in a multi-potential neural stem cell
TL;DR: It is shown here that elevated levels of cell-surface expression of DR5 and increased susceptibility to DR5-mediated apoptosis are characteristics of malignant tumor cells and selective, specific targeting ofDR5 with an agonistic antibody might be a safe and effective strategy for cancer therapy.
Abstract: A novel anti-human DR5 monoclonal antibody, TRA-8, induces apoptosis of most tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-sensitive tumor cells both in vitro and in vivo. In contrast to both the membrane-bound form of human TRAIL, which induced severe hepatitis in mice, and the soluble form of human TRAIL, which induced apoptosis of normal human hepatocytes in vitro, TRA-8 did not induce significant cell death of normal human hepatocytes. However, both primary hepatocellular carcinoma cells and an established liver cancer cell line were highly susceptible to the killing mediated by TRA-8. We show here that elevated levels of cell-surface expression of DR5 and increased susceptibility to DR5-mediated apoptosis are characteristics of malignant tumor cells. In contrast, DR5 alone is not sufficient to trigger apoptosis of normal hepatocytes. Therefore, selective, specific targeting of DR5 with an agonistic antibody might be a safe and effective strategy for cancer therapy.
TL;DR: This is the first knock-in mouse model of HD to show increased glial fibrillary acidic protein immunoreactivity in the striatum, suggesting that these mice have neuronal injury similar to that found early in the course of HD.
Abstract: Mice representing precise genetic replicas of Huntington's disease (HD) were made using gene targeting to replace the short CAG repeat of the mouse Huntington's disease gene homolog (HDH:) with CAG repeats within the length range found to cause HD in humans. Mice with alleles of approximately 150 units in length exhibit late-onset behavioral and neuroanatomic abnormalities consistent with HD. These symptoms include a motor task deficit, gait abnormalities, reactive gliosis and the formation of neuronal intranuclear inclusions predominating in the striatum. This model differs from previously described HDH: knock-ins by its method of construction, longer repeat length and more severe phenotype. To our knowledge, this is the first knock-in mouse model of HD to show increased glial fibrillary acidic protein immunoreactivity in the striatum, suggesting that these mice have neuronal injury similar to that found early in the course of HD. These mice will serve as useful reagents in experiments designed to reveal the molecular nature of neuronal dysfunction underlying HD.
TL;DR: It is reported here that the intracellular domain of Robo interacts with a novel family of Rho GTPase activating proteins (GAPs) that are expressed in regions responsive to Slit and demonstrated important roles for GAPs and Cdc42 in neuronal migration.
TL;DR: ReGel's inherent ability to solubilize (400 to >2000-fold) and stabilize poorly soluble and sensitive drugs, including proteins is a substantial benefit and the gel provided excellent control of the release of paclitaxel for approximately 50 days.
TL;DR: A case study of human immunodeficiency virus (HIV)-negative patients with cryptococcosis at 15 United States medical centers from 1990 through 1996 to understand the demographics, therapeutic approach, and factors associated with poor prognosis in this population as discussed by the authors.
Abstract: We conducted a case study of human immunodeficiency virus (HIV)-negative patients with cryptococcosis at 15 United States medical centers from 1990 through 1996 to understand the demographics, therapeutic approach, and factors associated with poor prognosis in this population. Of 306 patients with cryptococcosis, there were 109 with pulmonary involvement, 157 with central nervous system (CNS) involvement, and 40 with involvement at other sites. Seventy-nine percent had a significant underlying condition. Patients with pulmonary disease were usually treated initially with fluconazole (63%); patients with CNS disease generally received amphotericin B (92%). Fluconazole was administered to approximately two-thirds of patients with CNS disease for consolidation therapy. Therapy was successful for 74% of patients. Significant predictors of mortality in multivariate analysis included age > or =60 years, hematologic malignancy, and organ failure. Overall mortality was 30%, and mortality attributable to cryptococcosis was 12%. Cryptococcosis continues to be an important infection in HIV-negative patients and is associated with substantial overall and cause-specific mortality.
TL;DR: This review attempts to provide a critical description of some of the most common approaches to quantification of nitric oxide, superoxide, hydrogen peroxide, and peroxynitrite, with attention to key issues that may influence the utility of a particular assay when adapted for use in vascular cells and tissues.
Abstract: The evanescent nature of reactive oxygen and nitrogen species, the multiple cellular mechanisms evolved to maintain these substances at low (submicromolar) concentrations within the vascular system, and the often multifaceted nature of their reactivities have made measurement of these compounds within the vasculature problematic. This review attempts to provide a critical description of some of the most common approaches to quantification of nitric oxide, superoxide, hydrogen peroxide, and peroxynitrite, with attention to key issues that may influence the utility of a particular assay when adapted for use in vascular cells and tissues.
TL;DR: The objective was to determine whether 5% weight gain or loss in 3 years was predictive of mortality in a large sample of older adults.
Abstract: Objectives Previous studies of weight change and mortality in older adults have relied on self-reported weight loss, have not evaluated weight gain, or have had limited information on health status. Our objective was to determine whether 5% weight gain or loss in 3 years was predictive of mortality in a large sample of older adults. Design Longitudinal observational cohort study. Setting Four U.S. communities. Participants Four thousand seven hundred fourteen community-dwelling older adults, age 65 and older. Measurements Weight gain or loss of 5% in a 3-year period was examined in relationship to baseline health status and interim health events. Risk for subsequent mortality was estimated in those with weight loss or weight gain compared with the group whose weight was stable. Results Weight changes occurred in 34.6% of women and 27.3% of men, with weight loss being more frequent than gain. Weight loss was associated with older age, black race, higher weight, lower waist circumference, current smoking, stroke, any hospitalization, death of a spouse, activities of daily living disability, lower grip strength, and slower gait speed. Weight loss but not weight gain of 5% or more was associated with an increased risk of mortality that persisted after multivariate adjustment (Hazard ratio (HR) = 1.67, 95% CI = 1.29-2.15) and was similar in those with no serious illness in the period of weight change. Those with weight loss and low baseline weight had the highest crude mortality rate, although the HR for weight loss was similar for all tertiles of baseline weight and for those with or without a special diet, compared with those whose weight was stable. Conclusions This study confirms that even modest decline in body weight is an important and independent marker of risk of mortality in older adults.
TL;DR: The term DAI is a misnomer; it is not a diffuse injury to the whole brain, rather it is predominant in discrete regions of the brain following high-speed, long-duration deceleration injuries.
TL;DR: The WMFT is an instrument with high interrater reliability, internal consistency, test-retest reliability, and adequate stability, and is concluded to be an instrument that is suitable for assessing upper extremity motor function in adults with hemiplegia.