Miracle-dz/UniFAR-FTUs huggingface dataset:
Factors influencing mortgage valuation inaccuracy of residential property market within Kaduna Metropolis (Nigeria)

The measure of sale price of actual transaction of a particular property at a particular date and proximity is termed as valuation Accuracy. Errors contributing to this problem are Dearth of rental evidence, Inaccurate capitalization rate, Abodon of the correct procedures of arriving at opinion of values. The objective of this study is to identified factors that influence mortgage valuation inaccuracy in Kaduna Residential property market, also identify the acceptable margin of error in valuation among the practitioners in the study area as well as to develop a model of significant factors influencing valuation inaccuracy. A stratified sampling technique were used and a sample size of 67 respondents was determined using the sample size formula of Yamane (1968) of which were administered and only 51 were retrieved and analyzed. The study used multiple Regression Analysis (MRA), perception index Likert scale of measurement, with the aid of statistical package of social sciences (SPSS version 24). The key findings of the statistical analysis revealed that 16-20% percent was the perception of the valuers on the maximum acceptable margin of values in residential property valuation within the study area which is proxied to represent mortgage valuation inaccuracy. The findings also indicated, familiarity with property market, client pressure, Absence of national valuation standard, problem of relevant data, Regulatory framework and valuation methodology were the most contributing factors to valuation inaccuracy in the study area, while a model of significant factors contributing to valuation inaccuracy has been successfully developed to measure inaccuracy in valuation in the study area. Finally, this research will be of interest to the practitioners and academic researchers with an interest in mortgage valuation as an eye opener for employing accurate methods in conducting mortgage valuation in the study area.
Dynamic productivity growth and its determinants in the Indonesian food and beverages industry

ABSTRACT This research investigates dynamic productivity growth and its determinants in the Indonesian food and beverages industry decomposing dynamic productivity growth into the contributions of dynamic technical inefficiency change, dynamic technical change, and dynamic scale inefficiency change. The empirical application employs unbalanced panel data of 44 subsectors in the Indonesian food and beverages industry over 1990–2014. To estimate dynamic productivity growth, this research uses a Luenberger indicator accounting for the presence of adjustment costs. The results show that dynamic productivity growth exhibits a decreasing trend. Dynamic technical inefficiency change and dynamic scale inefficiency change contribute positively to dynamic productivity growth, while dynamic technical change contributes negatively. Dynamic productivity growth is affected by the change in industrial concentration, the growth rate of capital intensity, the growth rate of exports, the growth rate of foreign direct investment, and location.
Drug-resistant tuberculosis, clinical virulence, and the dominance of the Beijing strain family in Russia.

CONTEXT Tuberculosis and multidrug-resistant tuberculosis is a serious public health problem in Russia. OBJECTIVE To address the extent of "Beijing strain" transmission in the prison/civil sectors and the association of drug resistance, clinical, and social factors with the Beijing genotype. DESIGN AND SETTING Cross-sectional population-based molecular epidemiological study of all civilian and penitentiary tuberculosis facilities in the Samara region, Russia. PATIENTS Consecutively recruited patients with bacteriologically proven tuberculosis (n = 880). MAIN OUTCOME MEASURE Proportion of Beijing strains and association with drug resistance, human immunodeficiency virus infection, imprisonment, radiological, clinical, and other social factors. RESULTS Beijing-family strains (identified by spoligotyping and composed of 2 main types by mycobacterial interspersed repetitive unit analysis) were predominant: 586/880 (66.6%; 95% confidence interval [CI], 63.4%-69.7%) with a significantly higher prevalence in the prison population (rate ratio [RR], 1.3; 95% CI, 1.2-1.5) and those aged younger than 35 years (RR, 1.2; 95% CI, 1.0-1.3). Comparable proportions were co-infected with the human immunodeficiency virus ( approximately 10%), concurrent hepatitis B and C (21.6%), drank alcohol ( approximately 90%), smoked ( approximately 90%), and had a similar sexual history. Drug resistance was nearly 2-fold higher in patients infected with Beijing strains compared with non-Beijing strains: multidrug resistance (RR, 2.4; 95% CI, 1.9-3.0), for isoniazid (RR, 1.8; 95% CI, 1.5-2.1), for rifampicin (RR, 2.2; 95% CI, 1.7-2.7), for streptomycin (RR, 1.9; 95% CI, 1.5-2.3), and for ethambutol (RR, 2.2; 95% CI, 1.6-3.2). Univariate analysis demonstrated that male sex (odds ratio [OR], 1.5; 95% CI, 1.1-1.9), advanced radiological abnormalities (OR, 3.3; 95% CI, 1.3-8.4), homelessness (OR, 5.6; 95% CI, 1.1-6.3), and previous imprisonment (OR, 2.0; 95% CI, 1.5-2.7) were strongly associated with Beijing-strain family disease. Multivariate analysis supported previous imprisonment to be a risk factor (OR, 2.0; 95% CI, 1.4-3.3) and night sweats to be less associated (OR 0.7; 95% CI, 0.5-1.0) with Beijing-strain disease. CONCLUSIONS Drug resistance and previous imprisonment but not human immunodeficiency virus co-infection were significantly associated with Beijing-strain infection. There was evidence that Beijing isolates caused radiologically more advanced disease.
Plasmacytoid Dendritic Cells, Interferon Signaling, and FcγR Contribute to Pathogenesis and Therapeutic Response in Childhood Immune Thrombocytopenia

Targeting plasmacytoid dendritic cells or blockade of interferon response may benefit patients with an autoimmune disease against platelets. Type I Interferons—A Sticky Situation? “If you prick us, do we not bleed? ” – William Shakespeare One symptom of patients with low platelet numbers is not only do they bleed, they may have limited ability to stop bleeding. Immune thrombocytopenia (ITP) is one such disorder where the person’s own immune system attacks and destroys these critical clotting factors. Fortunately, infusion of intravenous immunoglobulins (IVIGs) can help to treat this disease. Now, Sehgal et al. shed some light on the mechanisms underlying both ITP pathogenesis and the effectiveness of IVIGs in ITP patients. The authors found that immune cells and plasma from ITP patients had increased amounts of type I interferons and downstream interferon response (IR) genes. Patients with therapy-induced remission lacked the increased IR signature. When treated with IVIG, monocytes from ITP patients altered the activating/inhibitory ratio of cell surface receptors that bind the Fc portion of IgG. These changes altered the ability of these cells to respond to type I interferon, and suggest that type I IR may contribute to ITP pathogenesis. Immune thrombocytopenia (ITP) is an autoimmune disorder of childhood characterized by immune-mediated destruction of platelets. The mechanisms underlying the pathogenesis of ITP and the therapeutic efficacy of intravenous immunoglobulins (IVIG) in this disorder remain unclear. We show that monocytes from patients with ITP have a distinct gene expression profile, with increased expression of type I interferon response (IR) genes. Plasma from ITP patients had increased levels of several cytokines indicative of immune activation, including an increase in interferon-α. ITP patients also had an increase in plasmacytoid dendritic cells (pDCs) compared to healthy donors. Therapy-induced remission of ITP was associated with abrogation of the IR gene signature in monocytes without reduction in the levels of circulating interferon-α itself. IVIG altered the ratio of activating/inhibitory Fcγ receptors (FcγRs) in vivo primarily by reducing FcγRIII (CD16). The engagement of activating FcγRs was required for IVIG-mediated abrogation of monocyte response to exogenous interferon-α in culture. Moreover, plasma from ITP patients led to activation of monocytes and myeloid DCs in culture with an increase in T cell stimulatory capacity; this activation depended on the engagement of activating FcγRs and interferon-α receptor (IFNAR) and was inhibited by antibody-mediated blockade of these pathways. These data point to a central role of type I interferon in the pathogenesis of ITP and suggest targeting pDCs and blockade of IR as potential therapeutic approaches in this disorder. They also provide evidence for the capacity of IVIG to extinguish IR in vivo, which may contribute to its effects in autoimmunity.
Rab11-FIP3 Regulation of Lck Endosomal Traffic Controls TCR Signal Transduction

The role of endosomes in receptor signal transduction is a long-standing question, which remains largely unanswered. The T cell Ag receptor and various components of its proximal signaling machinery are associated with distinct endosomal compartments, but how endosomal traffic affects T cell signaling remains ill-defined. In this article, we demonstrate in human T cells that the subcellular localization and function of the protein tyrosine kinase Lck depends on the Rab11 effector FIP3 (Rab11 family interacting protein-3). FIP3 overexpression or silencing and its ability to interact with Rab11 modify Lck subcellular localization and its delivery to the immunological synapse. Importantly, FIP3-dependent Lck localization controls early TCR signaling events, such as tyrosine phosphorylation of TCRζ, ZAP70, and LAT and intracellular calcium concentration, as well as IL-2 gene expression. Interestingly, FIP3 controls both steady-state and poststimulation phosphotyrosine and calcium levels. Finally, our findings indicate that FIP3 modulates TCR-CD3 cell surface expression via the regulation of steady-state Lck-mediated TCRζ phosphorylation, which in turn controls TCRζ protein levels. This may influence long-term T cell activation in response to TCR-CD3 stimulation. Therefore, our data underscore the importance of finely regulated endosomal traffic in TCR signal transduction and T cell activation leading to IL-2 production.
Induction of Receptor for Advanced Glycation End Products by EBV Latent Membrane Protein 1 and Its Correlation with Angiogenesis and Cervical Lymph Node Metastasis in Nasopharyngeal Carcinoma

Purpose: The EBV oncoprotein, latent membrane protein 1 (LMP1), contributes to the metastasis of nasopharyngeal carcinoma (NPC) by inducing factors to promote tumor invasion and angiogenesis. The receptor for advanced glycation end products (RAGE) is associated with abnormal angiogenesis in diabetic microangiopathies. Moreover, some papers have suggested the association of RAGE overexpression with tumor metastasis; thus, the associations of RAGE with LMP1 and angiogenesis in NPC were examined. Experimental Design: Forty-two patients with NPC were evaluated for expressions of LMP1, RAGE, and S100 proteins and for microvessel counts by immunohistochemistry. Then, the RAGE induction by LMP1 was examined with Western blotting and luciferase reporter assay. Results: The microvessel counts were significantly higher in patients with high LMP1 expression or high RAGE expression compared with cases with low expressions (P = 0.0049 and P < 0.0001), respectively. Patients with advanced N classification were also significantly increased in these groups (P = 0.0484 and P = 0.0005). The expressions of LMP1 and RAGE proteins were clearly correlated in NPC tissues (P = 0.0093). Transient transfection with LMP1 expression plasmid induced RAGE protein in Ad-AH cells. The expression of LMP1 transactivated the RAGE promoter as shown by luciferase reporter assay. Mutation of the reporter at nuclear factor-κB binding site (−671 to −663) abolished transactivation of the RAGE promoter by LMP1. Conclusion: These results suggest that LMP1-induced RAGE enhances lymph node metastasis through the induction of angiogenesis in NPC. Nuclear factor-κB binding site (−671 to −663) is essential for transactivation of the RAGE promoter by LMP1.
Role of human leukocyte antigen phenotype and exposure in development of occupational asthma

Studies of factory workforces in the past decade, exposed to both inhaled protein allergens (e.g. enzymes) and low molecular weight sensitisers (e.g. acid anhydrides), have provided consistent evidence of exposure-response relationships for both sensitisation (IgE production) and asthma. The development of molecular techniques has allowed investigation of candidate gene, in particular HLA Class 2 alleles, as risk factors contributing to individual susceptibility, in particular to low molecular weight chemicals. The frequency of HLA DR3 in cases of sensitisation to trimellitic anhydride and ammonium hexachloroplatinate is increased as compared to referents who have experienced a comparable intensity and duration of exposure. Similarly, HLA DQB1Asp57 is consistently more frequent in cases of isocyanate induced asthma. These observations indicate HLA Class 2 molecules contribute to individual susceptibility to sensitisation and asthma caused by low molecular weight chemicals. A study of platinum refinery workers suggested the relative risk associated with HLA phenotype was greater at lower levels of exposure.
Drug hypersensitivity in children: report from the pediatric task force of the EAACI Drug Allergy Interest Group

When questioned, about 10% of the parents report suspected hypersensitivity to at least one drug in their children. However, only a few of these reactions can be confirmed as allergic after a diagnostic workup. There is still a lack of knowledge on drug hypersensitivity (DH) epidemiology, clinical spectrum, and appropriate diagnostic methods particularly in children. Meanwhile, the tools used for DH management in adults are applied also for children. Whereas this appears generally acceptable, some aspects of DH and management differ with age. Most reactions in children are still attributed to betalactams. Some manifestations, such as nonsteroidal anti‐inflammatory drug‐associated angioedema and serum sickness‐like reactions, are more frequent among young patients as compared to adults. Risk factors such as viral infections are particularly frequent in children, making the diagnosis challenging. The practicability and validity of skin test and other diagnostic procedures need further assessment in children. This study presents an up‐to‐date review on epidemiology, clinical spectrum, diagnostic tools, and current management of DH in children. A new general algorithm for the study of these reactions in children is proposed. Data are presented focusing on reported differences between pediatric and adult patients, also identifying unmet needs to be addressed in further research.
Influence of prior cellular immunity on the in vitro lymphocyte response to virus antigens after influenza vaccination

The in vitro peripheral blood lymphocyte response to specific influenza virus antigens was studied before and 2 weeks after trivalent influenza vaccination of 16 healthy persons. Changes in serum hemagglutination inhibition antibody titers were also determined. An inverse correlation was found between the prevaccination antibody titers and the log2 mean-fold increase in antibody titers after vaccination (r = -0.86, P less than 0.01). An inverse correlation was also found between the prevaccination stimulation index and the ratio of postvaccination to prevaccination stimulation index for each virus strain (A/Victoria, r = -0.48, P less than 0.05; A/USSR, r = -0.55, P less than 0.02; and B/Hong Kong, r = -0.55, P less than 0.02). Similar negative correlations were not consistently found with the nonspecific mitogens phytohemagglutinin, pokeweed mitogen, and concanavalin A. These results suggest that the state of cellular as well as humoral immunity to virus antigens before vaccination influence the magnitude of response after vaccination and that antigen-specific suppressor cell activity may be stimulated by vaccination.
Localization of rRNA transcribed spacer domains in the nucleolinus and maternal procentrosomes of surf clam (Spisula) oocytes

The nucleolinus is a nuclear subcompartment long ago posited to play a role in cell division. In a recent study using surf clam oocytes, cytoplasmic foci containing a nucleolinar protein were shown to later recruit γ-tubulin, identifying them as centrosomal precursors.1 We now demonstrate the presence of structural RNAs from the nucleolinus in these procentrosomes. They include the well-known but poorly understood rRNA-transcribed spacer regions. In situ hybridization revealed a specific and dynamic association of these structural RNAs with the cell division apparatus that extends through the early stages of meiosis. In addition to their bearing on the debate over the nature of centrosome- and spindle-associated RNAs, the observations also suggest that rRNA spacer regions are not simply waste products to be discarded immediately, but may be functional byproducts that play a role in formation of the cell division apparatus.
Total absence of functional acid labile subunit, resulting in severe insulin-like growth factor deficiency and moderate growth failure.

CONTEXT Primary IGF deficiency (IGFD) describes the condition in which serum concentrations of IGF-I are low in the face of normal to elevated GH production. Because IGF-I, which circulates as part of a ternary complex with IGF binding protein (IGFBP)-3 and acid-labile subunit (ALS), mediates the growth-promoting effects of GH, IGFD is associated with severe growth failure in humans. OBJECTIVE We investigated a case of IGFD in which serum IGF-I and IGFBP-3 were abnormally low, yet growth failure was modest (-2.1 sd score at 15.5 yr of age). RESULTS The young male subject, from a consanguineous pedigree, had a postnatal growth profile consistently below the third percentile. The subject had a normal fasting GH level of 3.7 muU/ml and normal serum GH binding protein level (1258 pmol/liter; normal range 431-1892 pmol/liter), but serum IGF-I and IGFBP-3 were profoundly reduced (-5.8 and -7.2 sd score, respectively, at age 12.3 yr), even through puberty. A novel homozygous missense mutation was subsequently identified in the ALS gene, which resulted in severe deficiency of serum ALS (undetectable). CONCLUSIONS ALS is critical for maintaining normal serum concentrations of IGF-I and IGFBP-3, most likely by prolonging the half-lives of both proteins. ALS deficiency can be associated with moderate growth failure, but in this patient, the onset and progression of puberty appear to be normal. Altogether the results support a modest role for the ternary complex in the regulation of stature.
Transport mechanism and substrate specificity of human organic anion transporter 2 (hOat2 [SLC22A7])

Human organic anion transporter 2 (hOat2 [SLC22A7]) is highly expressed in the human liver. Although localization, gene expression, substrate specificity and transport mechanisms of other human Oat isoforms such as human Oat1 (hOat1), human Oat3 (hOat3) and human Oat4 (hOat4) have been elucidated, information concerning human Oat2 (hOat2) is less defined. The objective of this study was to provide further information on the transport mechanism and substrate specificity of hOat2. When expressed in Xenopus laevis oocytes, the transport of organic compounds mediated by hOat2 was not affected by the replacement of extracellular sodium with lithium, choline and mannitol. The uptake of estrone sulfate (ES) in hOat2‐expressing oocytes was significantly trans‐stimulated by preloading the oocytes with fumarate and succinate, but not glutarate. Moreover, we observed that hOat2 mediates the transport of bumetanide, ES, glutarate, dehydroepiandrosterone sulfate, allopurinol, prostaglandin E2, 5‐fluorouracil, paclitaxel and L‐ascorbic acid. These compounds are identified for the first time as hOat2 substrates. A wide range of structurally unrelated organic compounds inhibited the hOat2‐mediated uptake of tetracycline, except for sulfobromophthalein. All of these findings indicate that hOat2 is a sodium‐independent multi‐specific organic anion/dimethyldicarboxylate exchanger. Our present findings thus provide further insights into the role of hOat2 in hepatic drug transport.
Laparoscopic cholecystectomy can disseminate in situ carcinoma of the gallbladder.

BACKGROUND Early case reports suggest more frequent and rapid recurrences of carcinoma of the gallbladder after laparoscopic cholecystectomy (LC) than after open cholecystectomy. This cancer has a poor prognosis and occurs in 1 percent of patients who undergo cholecystectomies. STUDY DESIGN A recent community hospital series of gallbladder carcinoma (GBC) was reviewed and the total reported experience of GBC after LC was compiled. Diagnostic findings were compared for patients with GBC and a consecutive series of 24 patients who had LC for benign disease. RESULTS Nine patients with GBC were found among 928 patients who had undergone cholecystectomy (0.97 percent incidence). Compared to patients without GBC, patients with carcinoma were older, had thicker gallbladder walls, and had more abnormalities detected intraoperatively (all p < or = 0.05). Recurrence of GBC occurred more rapidly after LC, and in diffuse peritoneal and port sites when compared with recurrence patterns after open cholecystectomy. CONCLUSIONS In patients with GBC, LC may be sufficient when the disease is confined to the gallbladder mucosa and the gallbladder is excised intact without bile spillage. However, patients whose gallbladders are torn during dissection or patients who have invasive tumors should undergo laparotomy and local reexcision. In situ GBC can be implanted if the organ is torn during dissection. When gallbladders with suspicious wall thickening or adhesions are noted at LC, especially in older patients, the procedure should be converted to open cholecystectomy.
Role of the N‐terminal region of Rap1p in the transcriptional activation of glycolytic genes in Saccharomyces cerevisiae

In the yeast two‐hybrid system, the N‐terminal region of Rap1p was shown to interact with Gcr1p and Gcr2p. Disruption of gcr1 and/or gcr2 in the two‐hybrid reporter strain demonstrated that the interaction with Gcr1p does not require Gcr2p, whereas the interaction with Gcr2p is mediated through Gcr1p. Deletion of the N‐terminal region of Rap1p alone did not show a growth phenotype, but a growth defect was observed when this mutation was combined with a gcr2 deletion. The poor growth of the gcr1 null mutant was not affected further by the N‐terminal deletion of Rap1p, but the growth of gcr1 strains with mutations in the DNA binding region of Gcr1p was affected by the removal of the N‐terminal region of Rap1p. These results suggest that one function of the N‐terminal region of Rap1p, presumably the BRCT domain, is to facilitate the binding of Gcr1p to the promoter by a protein–protein interaction. Copyright © 2004 John Wiley & Sons, Ltd.