Miracle-dz/UniFAR-FTUs huggingface dataset:
Effects of protocol-driven care versus usual outpatient clinic care on survival rates in patients with type 2 diabetes.

OBJECTIVE To determine whether clinical outcomes in patients with type 2 diabetes were improved by protocol-driven care in a Diabetes Centre compared with usual outpatient care. STUDY DESIGN Descriptive analysis of a prospective cohort. PATIENTS AND METHODS During a median 7-year observational period, 91 patients with type 2 diabetes and no cardiovascular or renal complications were monitored by a nurse and a diabetologist in a clinical trial setting according to a structured protocol. Another 81 patients with comparable clinical characteristics were monitored by generalists at the medical clinic in the same hospital. Clinical end points, defined as death and cardiovascular and renal events, were evaluated in 1997 by review of case records. RESULTS Patients receiving structured care had lower mortality (relative risk [RR] = 0.21; 95% confidence interval [CI] = 0.07, 0.65; P = .006) than the usual-care group, as well as a lower incidence of combined clinical end points (RR = 0.43; 95% CI = 0.22, 0.84; P = .01). In the usual-care group, patients who had no monitoring of glycosylated hemoglobin or plasma lipid levels during the entire observational period (8.6%) had a 14.6-fold (P < .01) and 15.7-fold (P < .01) increased risk of death and combined clinical end points, respectively, compared with those who had at least one measurement (60.5%). CONCLUSION Management by protocol-driven care model improved survival and clinical outcomes in patients with type 2 diabetes. Definitive studies are required to confirm these findings and compare the cost effectiveness of these care models.
The effect of age on DNA concentration from whole saliva: Implications for the standard isolation method

Adequate quantity and quality of the DNA isolated from saliva samples are crucial for ensuring successful genotyping rates in genetic studies. However, there is little information about these issues when saliva samples are collected from children. The objectives of this study were to assess whether there are differences in DNA quality or quantity isolated from saliva samples of children at different ages and adolescents compared to adults and, if so, to establish a modified protocol to improve and standardize DNA isolation from saliva samples of children.
Tissue‐specific distribution and whole‐body burden estimates of persistent organic pollutants in the bottlenose dolphin (Tursiops truncatus)

Most exposure assessments for free‐ranging cetaceans focus on contaminant concentrations measured in blubber, and few data are available for other tissues or the factors governing contaminant distribution among tissues. The goal of this study was to provide a detailed description of the distribution of persistent organic pollutants (POPs) within the common bottlenose dolphin (Tursiops truncatus) body and assess the role of lipid dynamics in mediating contaminant distribution. Thirteen tissues (brain, blubber, heart, liver, lung, kidney, mammary gland, melon, skeletal muscle, spleen, thyroid, thymus, and testis/uterus) were sampled during necropsy from bottlenose dolphins (n = 4) and analyzed for lipid and 85 POPs, including polychlorinated biphenyls, organochlorine pesticides, and polybrominated diphenyl ethers. Significant correlations between tissue POP concentrations and lipid suggest that distribution of POPs is generally related to tissue lipid content. However, blubber:tissue partition coefficients ranged widely from 0.753 to 6.25, suggesting that contaminant distribution is not entirely lipid‐dependent. Tissue‐specific and whole‐body contaminant burdens confirmed that blubber, the primary site of metabolic lipid storage, is also the primary site for POP accumulation, contributing >90% to the whole‐body burdens. Observations also suggest that as lipid mobilizes from blubber, contaminants may redistribute, leading to elevated tissue concentrations. These results suggest that individuals with reduced blubber lipid may be at increased risk for exposure‐related health effects. However, this study also provides evidence that the melon, a metabolically inert lipid‐rich structure, may serve as an alternate depot for POPs, thus preventing the bulk of blubber contaminants from being directly available to other tissues. This unique physiological adaptation should be taken into consideration when assessing contaminant‐related health effects in wild cetacean populations. Environ. Toxicol. Chem. 2010;29:1263–1273. © 2010 SETAC
Systemic sclerosis in 3 US ethnic groups: a comparison of clinical, sociodemographic, serologic, and immunogenetic determinants.

OBJECTIVE To determine whether ethnic factors influence the presentation, serologic expression and immunogenetics of systemic sclerosis (SSc), patients from 3 ethnic groups were compared for clinical features, SSc-associated autoantibodies, and human leukocyte antigen (HLA) class II alleles. METHODS Fifty-four Hispanics, 28 African Americans, and 79 whites from Texas with recent-onset (less than 5 years) SSc enrolled in a prospective longitudinal study were assessed for sociodemographic, clinical, immunologic, immunogenetic, behavioral, and psychologic parameters using validated instruments and standard laboratory techniques. Serologic and immunogenetic characteristics from these patients and larger retrospective SSc cohorts of the same ethnic groups also were examined. RESULTS Hispanics and African Americans in the prospective cohort were more likely to have diffuse skin involvement, skin pigmentary changes, digital ulcers, pulmonary hypertension (African Americans), and an overall lower sociodemographic status than whites, who had more facial telangiectasia and hypothyroidism. In the larger combined prospective and retrospective groups of SSc patients, whites were likely to have more anticentromere antibodies (ACA) and African Americans more anti-U1-ribonucleoprotein (RNP) and anti-U3-RNP (fibrillarin) autoantibodies. HLA-DQB1*0301 was significantly associated with SSc per se in all 3 ethnic groups; HLA-DRB1*11 correlated with the anti-topoisomerase I antibody response, and HLA-DRB1*01, DRB1*04, and DQB1*0501 with ACA. CONCLUSIONS Important sociodemographic, clinical, and serologic differences exist between whites, African Americans, and Hispanics, despite shared genetic (HLA class II) predisposing factors. The impact of these differences on prognosis remain to be determined.
Papillary Renal Cell Carcinoma: Quantitation of Chromosomes 7 and 17 by FISH, Analysis of Chromosome 3p for LOH, and DNA Ploidy

Papillary renal cell carcinoma (papillary RCC) is an uncommon histologic variant of RCC with distinct gross, microscopic, and immunohistochemical features. Recent karyotypic analyses suggest that papillary RCC differs from other types of RCC at the genetic level as well. Whereas nonpapillary (clear cell, granular cell) RCC is characterized by deletions in chromosome 3p, papillary tumors reportedly exhibit a pattern of chromosomal trisomies, typically including chromosomes 7 and 17. To further examine the relationship between overrepresentation of these chromosomes and papillary histology, archival material from 36 papillary tumors was subjected to fluorescence in situ hybridization (FISH) analysis using α-satellite repeat probes specific to 7 and 17. Excess signals for chromosome 17 were detected in 22 of 28 (78%) low-grade papillary tumors (Fuhrman nuclear grades 1 and 2), and in seven of eight (87%) high-grade tumors (grades 3 and 4). Correlation of chromosome 17 FISH signals with karyotypes performed on two low-grade and three high-grade tumors was excellent. Among the cases without evidence of excess chromosome 17 were three unusual papillary tumors with sclerotic and hyalinized fibrovascular cores. In two cases, comparison was made of FISH signals from multiple, separate gross nodules of tumor; concordance for trisomic 17 signals was observed in one case, but not in the other. Chromosome 7 signals were overrepresented in all seven papillary tumors examined. DNA ploidy was determined in 19 of the 36 tumors; a relationship between DNA ploidy and polysomy 7 or 17 was not apparent. To examine the possible role of chromosome 3p deletions in the development of papillary RCC, 11 cases were studied for loss of heterozygosity (LOH) at one or more loci in the region of 3pl3–21. Only three of the 11 cases had LOH at these loci. The findings are discussed with respect to the development and progression of papillary RCC.
Fast skeletal muscle troponin T increases the cooperativity of transgenic mouse cardiac muscle contraction

1 To investigate the functional significance of different troponin T (TnT) isoforms in the Ca2+ activation of muscle contraction, transgenic mice have been constructed with a chicken fast skeletal muscle TnT transgene driven by a cardiac α‐myosin heavy chain gene promoter. 2 Cardiac muscle‐specific expression of the fast skeletal muscle TnT has been obtained with significant myofibril incorporation. Expression of the endogenous cardiac muscle thin filament regulatory proteins, such as troponin I and tropomyosin, was not altered in the transgenic mouse heart, providing an authentic system for the functional characterization of TnT isoforms. 3 Cardiac muscle contractility was analysed for the force vs. Ca2+ relationship in skinned ventricular trabeculae of transgenic mice in comparison with wild‐type litter‐mates. The results showed unchanged pCa50 values (5.1 ± 0.04 and 5.1 ± 0.1, respectively) but significantly steeper slopes (the Hill coefficient was 2.0 ± 0.2 vs. 1.0 ± 0.2, P < 0.05). 4 The results demonstrate that the structural and functional variation of different TnT isoforms may contribute to the difference in responsiveness and overall cooperativity of the thin filament‐based Ca2+ regulation between cardiac and skeletal muscles.
Promotion of functioning of human periodontal ligament cells and human endothelial cells by nerve growth factor.

BACKGROUND We have previously shown that cultured human periodontal ligament (HPL) cells produce nerve growth factor (NGF) and express mRNA of tyrosine kinase receptor (trkA), a high-affinity receptor of NGF. These findings suggest that NGF modulates the differentiation and proliferation of the periodontal ligament cells by paracrine and autocrine functions in vivo. Endothelial cells also express NGF and trkA. Therefore, NGF may regulate functions of periodontal ligament cells and endothelial cells during periodontal tissue regeneration. METHODS Effects of NGF on expressions of bone/cementum-related proteins (osteocalcin [OC], bone sialoprotein [BSP], bone morphogenetic protein [BMP-7], core binding factor alpha [Cbfa-1], and type I collagen), calcification in HPL cells, and proliferation and mRNA expression of vascular endothelial growth factor (VEGF), an endothelial cell mitogen, in human microvascular endothelial cells (HMVECs) were examined. RESULTS NGF elevated mRNA levels of OC, BSP, BMP-7, Cbfa-1, and type I collagen and enhanced mineral deposition in cultures of HPL cells. Furthermore, NGF stimulated mRNA expressions of VEGF-A and VEGF-B and cell proliferation in HMVEC. CONCLUSION These findings suggest that the functional regulation of periodontal ligament cells and endothelial cells by NGF might result in the acceleration of periodontal tissue regeneration in vivo.
New England medical center posterior circulation registry

Among 407 New England Medical Center Posterior Circulation registry patients, 59% had strokes without transient ischemic attacks (TIAs), 24% had TIAs then strokes, and 16% had only TIAs. Embolism was the commonest stroke mechanism (40% of patients including 24% cardiac origin, 14% intraarterial, 2% cardiac and arterial sources). In 32% large artery occlusive lesions caused hemodynamic brain ischemia. Infarcts most often included the distal posterior circulation territory (rostral brainstem, superior cerebellum and occipital and temporal lobes); the proximal (medulla and posterior inferior cerebellum) and middle (pons and anterior inferior cerebellum) territories were equally involved. Severe occlusive lesions (>50% stenosis) involved more than one large artery in 148 patients; 134 had one artery site involved unilaterally or bilaterally. The commonest occlusive sites were: extracranial vertebral artery (52 patients, 15 bilateral) intracranial vertebral artery (40 patients, 12 bilateral), basilar artery (46 patients). Intraarterial embolism was the commonest mechanism of brain infarction in patients with vertebral artery occlusive disease. Thirty‐day mortality was 3.6%. Embolic mechanism, distal territory location, and basilar artery occlusive disease carried the poorest prognosis. The best outcome was in patients who had multiple arterial occlusive sites; they had position‐sensitive TIAs during months to years. Ann Neurol 2004;56:389–398
Vascular Endothelial-Junctional Adhesion Molecule (VE-JAM)/JAM 2 Interacts with T, NK, and Dendritic Cells Through JAM 3

Screening expressed sequence tag databases for endothelial-specific homologs to human junctional adhesion molecule (JAM) and A33-Ag, we identified a protein of 298 aa that represents the recently described vascular endothelial-JAM (VE-JAM)/JAM 2. We confirmed VE-JAM/JAM 2 expression to be restricted to the high endothelial venule of tonsil and lymph nodes, and we further expanded the localization to the endothelium of arterioles in and around inflammatory and tumor foci. In our functional characterizations of VE-JAM/JAM 2, we discovered that it can function as an adhesive ligand for the T cell line J45 and can interact with GM-CSF/IL-4-derived peripheral blood dendritic cells, circulating CD56+ NK cells, circulating CD56+CD3+ NK/T cells, and circulating CD56+CD3+CD8+ cytolytic T cells. In the course of our studies, we also isolated and characterized the functional VE-JAM/JAM 2 receptor, which, upon cloning, turned out to be a submitted sequence representing JAM 3 (accession number NP 113658). With these understandings, we have characterized a protein-interacting pair that can be important in the role of T, NK, and dendritic cell trafficking and inflammation.
Children's Yale-Brown Obsessive Compulsive Scale: reliability and validity.

OBJECTIVE To evaluate the reliability and validity of a semistructured measure of obsessive-compulsive symptom severity in children and adolescents with obsessive-compulsive disorder (OCD). METHOD Sixty-five children with OCD (25 girls and 40 boys, aged 8 to 17 years) were assessed with the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS). Interrater agreement was assessed by four raters in a subsample (n = 24). Discriminant and convergent validity were assessed by comparing CY-BOCS scores to self-ratings of depression, anxiety, and obsessive-compulsive symptoms. RESULTS Internal consistency was high, measuring . 87 for the 10 items. The intraclass correlations for the CY-BOCS Total, Obsession, and Compulsion scores were . 84, . 91, and . 68, suggesting good to excellent interrater agreement for subscale and total scores. The CY-BOCS Total score showed a significantly higher correlation with a self-report of obsessive-compulsive symptoms (r = .62 for the Leyton survey) compared with the Children's Depression Inventory (r = .34) and the Children's Manifest Anxiety Scale (r = .37) (p = .02 and .05, respectively). CONCLUSIONS The CY-BOCS yields reliable and valid subscale and total scores for obsessive-compulsive symptom severity in children and adolescents with OCD. Reliability and validity appear to be influenced by age of the child and the hazards associated with integrating data from parental and patient sources.
Are you sure your software is gender-neutral?

the optimal representation of women in groups and how to achieve it. These are worthwhile topics for discussion, but I want to take the conversation in a different direction. I don't want to see women missing out on great technologies while we wait for the pipeline of female candidates to fill, and I don't want businesses missing out on being successful in the marketplace by not successfully creating products and services for 51 percent of the population [2]. Frequently, products are built with the assumption that they are gender-neutral; no gender is intentionally assigned to their users. But this does Women account for 50 percent of people on payroll [1] and account for even greater purchasing power. Some products (all too often pink) are deliberately built for a female audience, and some are built for a male audience. However, many products are intended to be gender-neutral. Here, I address the latter and ask, exactly how well designed are these supposedly gender-neutral products? Many papers focus on ways to increase the participation of women in computer science and the challenge of channeling more female candidates into IT positions. There is endless talk Insights → Unintended gender bias can show up at any point in the product cycle. → Feminine perspectives rarely get shared in current engineering practices. → Integrating inexpensive approaches into engineering practices can reduce unintended gender bias.
Lymphocyte Apoptosis and Thrombocytopenia in Spleen during Classical Swine Fever: Role of Macrophages and Cytokines

Thirty-two Large White X Landrace pigs, 4 months old, were inoculated with the classical swine fever (CSF) or hog cholera virus strain “Alfort” in order to identify the mechanism responsible for the lymphopenia and thrombocytopenia observed in the spleen during the experimental induction of disease, by immunohistochemical and ultrastructural techniques. Results showed a progressive depletion of splenic lymphoid structures and evidence of platelet aggregation processes. Lymphoid depletion was due to lymphocyte apoptosis, which could not be ascribed to the direct action of the virus on these cells; direct virus action could play only a secondary role in the death of these cells. Absence of severe tissue and endothelial damage, together with moderate procoagulant cytokine levels in the serum, suggest that these pathologies can be ruled out as the cause of platelet aggregation and thrombocytopenia in CSF. Monocyte/macrophages were the main target cells for the CSF virus, and they exhibited phagocytic and secretory activation leading to the synthesis and release of tumor necrosis factor α, which proved to be the chief mediator, followed by IL-6, IL-1α, and C1q complement component. In view of their characteristics, TNF-α and, to a lesser extent, IL-1α and IL-6 appear to be the major cytokines involved in the pathogenesis of lymphocytopenia and thrombocytopenia; a clear spatial and temporal relationship was observed between these two phenomena.
Evaluation of Short-Term Outcome after Lung Transplantation in the Lung Allocation Score Era

Abstract Background In December 2011, the Eurotransplant Foundation (Leiden, The Netherlands) changed the allocation system for donor lungs from a model based on urgency and waiting time to the lung allocation score (LAS). Objective The aim of the study was to investigate the effects of the LAS implementation on the early outcome after lung transplantation in Germany. Methods We therefore retrospectively studied the outcome of the last 50 patients transplanted before and the first 50 patients transplanted after LAS implementation. Results Both patient groups were comparable in baseline characteristics at the time of transplantation. Postoperative hospital stays were comparable between the groups, that is, 40.3 ± 26.8 and 40.3 ± 31.3 days (p = 0.992). Also, survival rates on intensive care, during entire hospital stay, at 90 days, 6 month, and 1 year after transplant were comparable between the groups. The retrospectively calculated LASs of the patients transplanted under the old allocation system were not statistically significantly different from those after LAS implementation, that is, 46.5 ± 14.2 and 51.2 ± 17.4 (p = 0.139). Conclusion We demonstrate, for the first time, that implementation of the LAS in Germany had no negative effect on the early outcome after lung transplantation. Our data indicate that patients transplanted before implementation of the LAS had a similar prospective transplant benefit.
Estimating progression to cirrhosis in chronic hepatitis C virus infection

To gain a clearer understanding of the rate of progression to cirrhosis and its determinants in chronic hepatitis C virus (HCV) infection, a systematic review of published epidemiologic studies that incorporated assessment for cirrhosis has been undertaken. Inclusion criteria were more than 20 cases of chronic HCV infection, and information on either age of subjects or duration of infection. Of 145 studies examined, 57 fulfilled the inclusion criteria. Least‐squares linear regression was employed to estimate rates of progression to cirrhosis, and to examine for factors associated with more rapid disease progression in 4 broad study categories: 1) liver clinic series (number of studies = 33); 2) posttransfusion cohorts (n = 5); 3) blood donor series (n = 10); and 4) community‐based cohorts (n = 9). Estimates of progression to cirrhosis after 20 years of chronic HCV infection were 22% (95% CI, 18%‐26%) for liver clinic series, 24% (11%‐37%) for posttransfusion cohorts, 4% (1%‐7%) for blood donor series, and 7% (4%‐10%) for community‐based cohorts. Factors that were associated with more rapid disease progression included older age at HCV infection, male gender, and heavy alcohol intake. Even after accounting for these factors, progression estimates were much higher for cross‐sectional liver clinic series. Selection biases probably explain the higher estimates of disease progression in this group of studies. Community‐based cohort studies are likely to provide a more representative basis for estimating disease progression at a population level. These suggest that for persons who acquire HCV infection in young adulthood, less than 10% are estimated to develop cirrhosis within 20 years. (HEPATOLOGY 2001;34:809‐816.)
Alterations in CDKN2A locus as potential indicator of melanoma predisposition in relatives of non-familial melanoma cases.

AIM To examine constitutional alterations of CDKN2A/p16INK4A locus as a potential indicator of melanoma predisposition among the first-degree relatives of patients with malignant melanoma. METHOD The study included eight families with a single member affected with melanoma. Members of the families were screened for allelic cosegregation with 9p21 region polymorphic markers IFNA, D9S126, and D9S104. The patient's tumors were screened for loss of heterozygosity (LOH) with the same markers, as well as for single strand conformational polymorphism (SSCP) variability of CDKN2A. In suspect cases, constitutional DNA was examined by SSCP and direct sequencing. RESULTS LOH was detected in four cases, and SSCP indicated variability in at least one CDKN2A exon in these tumor samples. In three of four LOH cases, the remaining allele cosegregated within the family, which was interpreted as a preliminary indicator of potential genetic predisposition. In one of these three families, we found constitutional CDKN2A mutations in the patient and one of the relatives. In the second family, only the patient had the constitutionally altered gene, whereas no constitutional CDKN2A alterations were detected in the third family. All significant mutations were different and had not been reported before. CONCLUSION We detected one case of melanoma predisposition among unaffected family members, which corresponded to statistical expectations for such a small number of screened families. Since constitutional mutations of CDKN2A exons have limited incidence, our stepwise approach seemed to be more informative and more affordable than straightforward CDKN2A sequencing of all subjects.