Miracle-dz/UniFAR-FTUs huggingface dataset:
Strategies to Increase Farmers' Financial Inclusion

This research aims to determine the level of interest by farmers in using theservices of formal financial institutions, especially digital financial services(DFS). The methods of the research were descriptive statistics and SEM analysis.The majority of respondents (50%) farmed an average area of land less than0.5 hectares, 26% of respondents an average of 0.75-1 hectares and 24% ofrespondents an average of 0.5-0.75 hectares of land. Based on the status of landownership, nas many as 76% of nrespondents owned the property itself, 19% hada lleaser arrangement and 5% used state owned larablerland. A total of 27% ofthe farmers were interested in using DFS while 34% were not. The lack of interesetwas due to practical uses, enjoyment of cash and lack of knowledge. The reasonfor interest in DFS included practicality, speed, and security of use. Results fromthe SEM model indicate a significant and positive influence of Access to Usage,significant and negative influence of DFS to Access, significant and positiveinfluence of DFS to Interest, significant and positive of Interest to Desire, and asignificant and positive Desire to Access.
Plakoglobin is essential for myocardial compliance but dispensable for myofibril insertion into adherens junctions

Plakoglobin (γ‐catenin), a member of the armadillo family of proteins, is a constituent of the cytoplasmic plaque of cardiac junctions and is involved in anchorage of cytoskeletal filaments to specific cadherins. Its genetic inactivation leads to an embryonic lethal phenotype due to heart dysfunction related to an impairment in the architecture of intercalated discs and in the stability of the heart tissue. To elucidate the functional consequences of the loss of plakoglobin for myofibrillar function, we monitored passive stress–strain relationship and contractility parameters of demembranated embryonic fibers. Heart fibers obtained from plakoglobin‐deficient embryonic mice were significantly less compliant than were fibers from wild‐type embryos. This difference was especially pronounced at lower fiber extension levels: at 120% of slack length, compliance was 2.5‐fold lower in plakoglobin‐deficient mice than in the corresponding wild‐type group. Contractile paramenters (force per cross‐section; Ca2+ sensitivity of isometric force and shortening velocity at near‐zero load) were comparable in all experimental groups. Therefore, we suggest that plakoglobin is important for cardiac compliance but not necessary for the attachment of the myofibrillar apparatus to adherens junctions. Thus, we conclude that the loss of function of desmosomes and the profound disarrangement of junctional components in plakoglobin null embryos is associated with a decreased passive compliance, which may explain the ventricular rupture and consequent pericardial tamponade in embryos lacking plakoglobin. J. Cell. Biochem. 72:8–15, 1999. © 1999 Wiley‐Liss, Inc.
Enterprise Models in Terms of Sustainability

The economy, with its driving forces, operating conditions and the consumers’ motivation, plays the determining role in the forming of sustainability. The present paper examines a narrower issue within this: the structure of an enterprise model that can be operated in accordance with the requirements of sustainability. The examined model variants essentially differ in risk holder types. The paper discusses two very important criteria of matching to sustainability. On one hand, the smooth operation of the company should not require the existence of the natural rate of unemployment; on the other hand, the driving force related to the success of the enterprise should remain within the company. The model where these two requirements are met concurrently is the working people’s enterprise basic model. When the two criteria mentioned above are met, various model variants may be viable. The presentation of the operating conditions and operating mechanisms of these models can build new aspects in the process of sustainability research.
White Spot Syndrome Virus Induces Metabolic Changes Resembling the Warburg Effect in Shrimp Hemocytes in the Early Stage of Infection

ABSTRACT The Warburg effect is an abnormal glycolysis response that is associated with cancer cells. Here we present evidence that metabolic changes resembling the Warburg effect are induced by a nonmammalian virus. When shrimp were infected with white spot syndrome virus (WSSV), changes were induced in several metabolic pathways related to the mitochondria. At the viral genome replication stage (12 h postinfection [hpi]), glucose consumption and plasma lactate concentration were both increased in WSSV-infected shrimp, and the key enzyme of the pentose phosphate pathway, glucose-6-phosphate dehydrogenase (G6PDH), showed increased activity. We also found that at 12 hpi there was no alteration in the ADP/ATP ratio and that oxidative stress was lower than that in uninfected controls. All of these results are characteristic of the Warburg effect as it is present in mammals. There was also a significant decrease in triglyceride concentration starting at 12 hpi. At the late stage of the infection cycle (24 hpi), hemocytes of WSSV-infected shrimp showed several changes associated with cell death. These included the induction of mitochondrial membrane permeabilization (MMP), increased oxidative stress, decreased glucose consumption, and disrupted energy production. A previous study showed that WSSV infection led to upregulation of the voltage-dependent anion channel (VDAC), which is known to be involved in both the Warburg effect and MMP. Here we show that double-stranded RNA (dsRNA) silencing of the VDAC reduces WSSV-induced mortality and virion copy number. For these results, we hypothesize a model depicting the metabolic changes in host cells at the early and late stages of WSSV infection.
Identification of L-ferritin in Neuromelanin Granules of the Human Substantia Nigra

In the pigmented dopaminergic neurons of the human substantia nigra pars compacta the system relevant in iron storage is the polymer neuromelanin (NM). Although in most cells this function is mainly accomplished by ferritin, this protein complex appears not to be expressed in NM-containing neurons. Nevertheless the conceivable presence of iron-storing proteins as part of the NM granules has recently been discussed on the basis of Mössbauer spectroscopy and synchrotron x-ray microspectroscopy. Intriguingly by combining subcellular fractionation of NM granules, peptide sequencing via tandem mass spectrometry, and the additional confirmation by multiple reaction monitoring and immunogold labeling for electron microscopy, L-ferritin could now be unambiguously identified and localized in NM granules for the first time. This finding not only supports direct evidence for a regulatory role of L-ferritin in neuroectodermal cell pigmentation but also integrates a new player within a complicated network governing iron homeostasis in the dopamine neurons of the human substantia nigra. Thus our finding entails far reaching implications especially when considering etiopathogenetic aspects of Parkinson disease.
Ion-Trapping, Microsomal Binding, and Unbound Drug Distribution in the Hepatic Retention of Basic Drugs

This study investigated the relative contribution of ion-trapping, microsomal binding, and distribution of unbound drug as determinants in the hepatic retention of basic drugs in the isolated perfused rat liver. The ionophore monensin was used to abolish the vesicular proton gradient and thus allow an estimation of ion-trapping by acidic hepatic vesicles of cationic drugs. In vitro microsomal studies were used to independently estimate microsomal binding and metabolism. Hepatic vesicular ion-trapping, intrinsic elimination clearance, permeability-surface area product, and intracellular binding were derived using a physiologically based pharmacokinetic model. Modeling showed that the ion-trapping was significantly lower after monensin treatment for atenolol and propranolol, but not for antipyrine. However, no changes induced by monensin treatment were observed in intrinsic clearance, permeability, or binding for the three model drugs. Monensin did not affect binding or metabolic activity in vitro for the drugs. The observed ion-trapping was similar to theoretical values estimated using the pHs and fractional volumes of the acidic vesicles and the pKa values of drugs. Lipophilicity and pKa determined hepatic drug retention: a drug with low pKa and low lipophilicity (e.g., antipyrine) distributes as unbound drug, a drug with high pKa and low lipophilicity (e.g., atenolol) by ion-trapping, and a drug with a high pKa and high lipophilicity (e.g., propranolol) is retained by ion-trapping and intracellular binding. In conclusion, monensin inhibits the ion-trapping of high pKa basic drugs, leading to a reduction in hepatic retention but with no effect on hepatic drug extraction.
Racial and Ethnic Variation in the Predictors of Maternal Parenting Stress

ABSTRACT Little is known about racial and ethnic disparities in maternal parenting stress. Using Belsky's (1984) conceptual model, which characterizes parenting stress as a function of maternal and child characteristics and social context, we examine determinants of parenting stress among Mexican American mothers in comparison to non-Hispanic White and non-Hispanic Black mothers. Using data from the Fragile Families and Child Well-Being (FFCWB) Study, we analyze a sample of 2,898 mothers. According to our findings, patterns of parenting stress for non-Hispanic White and non-Hispanic Black mothers are fairly consistent with Belsky's model. However, for Mexican American mothers, social support, but not partner support, ameliorates parenting stress, and depression is not associated with parenting stress. Importantly, despite significant social disadvantage, parenting stress levels in Mexican American mothers do not significantly differ from those of non-Hispanic Whites. Specific recommendations are made to practitioners for culturally competent responses to parenting stress with Mexican American families.
Evaluation of hypertension by the general pediatrician

Purpose of review To summarize the recommended work-up in a child who presents with elevated blood pressure as well as innovative evaluation techniques under development. Recent findings ‘The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents’ contains several updates on the diagnosis, evaluation and treatment of childhood hypertension. New risk factors for hypertension have been identified and include obesity, sleep apnea, and low birth weight. The roles of uric acid, leptin and C-reactive protein in the pathophysiology of hypertension have been examined. The presence of hypertensive end-organ damage has been demonstrated in hypertensive children. Summary Current knowledge emphasizes the need to diagnose and treat hypertension when it develops in childhood to decrease the risk of cardiovascular morbidity in adulthood. End-organ injury is evident, illustrated by the presence of left ventricular hypertrophy, even in young children. Assessment for the presence of comorbidities and end-organ damage should be emphasized. Further study is needed to isolate the etiologic factors for childhood hypertension, improve evaluation techniques, and determine if end-organ damage is reversible with proper therapy.
Distributed connectivity control in a dynamic network

In this paper, we propose a distributed algorithm to control connectivity of mobile agents in a constrained dynamic network. The connectivity property of the multi-agent system is quantified by the second smallest eigenvalue of the state dependent Laplacian of the proximity graph of agents. Motivated by k-regular graph characteristics, we consider a discrete-time model for autonomous agents. We explore an approach based on tentative overlay as a condition mapping from interrelation and interaction between each agent, which equipped with local sensing and wireless communication capabilities. It thereby shows that load balancing can be controlled with network's connectivity, while other than nearest neighbor information, our approach assumes no knowledge of global network topology. Simultaneously, a new collision avoidance method motivated by vertex coloring is presented for our distributed approach. In addition, simulations are provided that demonstrate the effectiveness of our theoretical results, for which we show a distributed dynamic programming of multi-agent system.
Long-term metabolic consequences of being born small for gestational age

During the last 15 years, a number of long-term health risks associated with reduced fetal growth have been identified, including cardiovascular diseases and the insulin-resistance syndrome or one of its components: hypertension, dyslipidemia, impaired glucose tolerance or Type 2 diabetes. A common feature of these conditions is the presence of high insulin levels, which are thought to play a pathogenic role. However, despite abundant data in the literature, it is still difficult to trace the pathway by which fetal events, environmental or not, may lead to the increased morbidity later in life. To explain this association, several hypotheses have been proposed pointing to the critical role of either a detrimental fetal environment or a genetic susceptibility, or indicating interaction of both. Clearly, not all subjects born small for gestational age are at the same risk of developing these complications. It appears that individuals at particular risk are those who were thin at birth and had a subsequent catch-up in body mass index, irrespective of the degree of adiposity in adulthood. It is suggested that this particular dynamic change in adiposity has a critical role in the development of long-term metabolic complications. Therefore, it is important to consider the relative impact of early postnatal events in relation to fetal growth to the diseases risk throughout life in forming health policy strategies towards eventual early interventions.
Sequential Parenteral to Oral Clindamycin Dosing in Pediatric Musculoskeletal Infection: A Retrospective Review of 30 mg/kg/d Versus 40 mg/kg/d

Background: Children with musculoskeletal infection in methicillin-resistant Staphylococcus aureus (MRSA) prevalent communities are often treated with oral clindamycin. Current guidelines recommend approximately 40 mg/kg/d for MRSA infections. This study investigates the clinical practice of using 30 mg/kg/d of clindamycin as an alternative for outpatient dosing. Methods: Children with musculoskeletal infection treated with outpatient clindamycin from 2009 to 2014 were studied by retrospective review. The amount of clindamycin administered was determined from dose, interval and duration of outpatient treatment. Hospital readmission, surgeries and sequelae were assessed. Severity of illness was determined for children with osteomyelitis. The readmission rate of 25 children treated with 40 mg/kg/d was compared with that of 190 children treated with 30 mg/kg/d. The reason for readmission was evaluated to consider whether antibiotic dosing strategy was a potential factor. Results: Among 215 children studied, the average outpatient duration of treatment was 32.8 days. There was no significant difference in the rate of readmission between dosing cohorts. Severity of illness scores (0–10 scale) was significantly higher among readmitted children with osteomyelitis (mean 9.8 ± 0.4) than among those with osteomyelitis who were not readmitted (mean 2.9 ± 3.2), P = 0.001. Sequelae were more common in the high-dose group and were noted in 3 children (12%) in that cohort compared with 6 children (3.2%) in the low-dose cohort (P > 0.05). Conclusion: Oral dosing of 30 mg/kg/d was effective for musculoskeletal infection in children in an MRSA prevalent community. Illness severity appeared to have greater impact on readmission and sequelae than did antibiotic dosing.
[Psychotic experiences in the course of alcohol withdrawal symptoms: locus of control among patients with and without delirium and analysis of subjective experiences in delirium].

AIM The comparison of the locus of control in groups of patients hospitalised due to alcohol withdrawal with and without delirium and analysis of psychotic experiences of patients with delirium. METHODS 25 patients with alcohol withdrawal with delirium and 25 without delirium took part in the study. They filled-in the Internal-External (I-E) Locus of Control Scale by Rotter; Multidimensional Health Locus of Control (MHLC) scale; the group with delirium also did the Psychopathological Symptoms Inventory, by Bizoń et al. RESULTS The mean score in I-E Locus of Control Scale in the group with delirium was more external than in the group without delirium (M = 13.28; SD = 2.762 versus M = 11.64; SD = 2.612; t(48) = -2.157; p = 0.036). Group with delirium had also lower mean score in the dimension of internal control in MHLC, than the group without delirium (M = 24.8; SD = 6.149 versus M = 26.8; SD = 4.648; t(48) = 1.99; p = 0.04). There were no statistically significant differences between the groups in the other subscales. The auditory and visual hallucinations were most common among patients with delirium (84%, 80% respectively, as well as delusions of taking part in not existing events (92%) and persecutory delusions (80%). Psychotic experiences influenced behaviour in nearly 50% of the cases. CONCLUSIONS A more external locus of control may be one of the factors contributing to the development of alcohol delirium. The content of psychotic experiences seems to have impact on the behaviour of many patients with alcohol delirium.
Higher triglycerides, lower high-density lipoprotein cholesterol, and higher systolic blood pressure in lipoprotein lipase-deficient heterozygotes. A preliminary report.

BACKGROUND Heterozygous lipoprotein lipase (LPL) deficiency has been associated with familial hypertriglyceridemia and familial combined hyperlipidemia. Studies of heterozygotes with LPL gene defects at amino acid residues 188 and 207 showed higher triglycerides (TG) and lower HDL cholesterol (HDL-C), with no elevation in LDL cholesterol (LDL-C). Other LPL defects may reveal alternate clinical phenotypes. METHODS AND RESULTS We evaluated three families with defects at amino acid residues 64, 194, and 188. Thirty-eight heterozygotes (8 with defect 64, 14 with defect 194, and 16 with defect 188) and 95 family members without defects were studied. Plasma lipid, lipoprotein, and apolipoprotein (apo) values were measured, as well as blood pressure. Pooled carriers demonstrated higher systolic blood pressure (SBP) (127 versus 116 mm Hg, P < .0001) and TG (160 versus 125 mg/dL, P = .004) and lower HDL-C (44 versus 52 mg/dL, P = .001) than did noncarriers. A comparison of the 188 carriers and noncarriers revealed the most striking phenotypic characteristics, with lower HDL-C (36 versus 51 mg/dL, P < .0001) and HDL-C/(apo A-I + apo A-II) (0.21 versus 0.24, P = .002) and higher TG (206 versus 123 mg/dL, P = .0003), SBP (132 versus 116 mm Hg, P = .0004), and apo B/LDL-C (1.12 versus 0.93, P < .0001). CONCLUSIONS These data confirm past observations that LPL deficient heterozygotes trend toward lower HDL-C and higher TG levels while potentially expressing higher SBP. These data also implicate the specific LPL gene defect as a contributing factor to the variable expression of HDL-C, TG, and SBP.
Impact of cytomegalovirus serostatus on outcome of unrelated cord blood transplantation for adults: a single‐institute experience in Japan

Cytomegalovirus (CMV) disease is one of the major infectious complications after allogeneic hematopoietic stem cell transplantation (SCT). Several studies have shown that CMV‐seropositive patients have a substantial survival disadvantage after bone marrow transplantation (BMT) or peripheral blood SCT (PBSCT). Between August 1998 and February 2006, 101 adult patients underwent myeloablative cord blood transplantation (CBT) from unrelated donors at our institution. Sixteen and 85 patients were CMV‐seronegative and CMV‐seropositive, respectively, prior to CBT. Outcomes of CBT were compared between CMV‐seronegative and CMV‐seropositive patients. The cumulative incidences of neutrophil engraftment at 60 d after CBT did not differ between CMV‐seronegative and CMV‐seropositive patients (100% and 94%, P = 0.09); however, the cumulative incidence of platelet engraftment at 100 d was higher in CMV‐seronegative patients than CMV‐seropositive patients (100% vs. 86%, P < 0.005). The cumulative incidence of CMV antigenemia at 100 d was lower in CMV‐seronegative patients than CMV‐seropositive patients (0% vs. 77%, P < 0.001); however, the cumulative incidences of CMV disease did not differ between CMV‐seronegative and CMV‐seropositive patients (0% vs. 1%, P = 0.84). The probabilities of disease‐free survival at 2 yr also did not differ between CMV‐seronegative and CMV‐seropositive patients (92% vs. 72%, P = 0.16). The outcomes of CBT for CMV‐seropositive patients as well as CMV‐seronegative patients in our series were favorable. This might be due to effective antiviral therapy for CMV infection. Large‐scale studies are needed to determine the impact of recipient CMV serostatus on the outcome of CBT for adults.
Effect of Losartan Therapy on Endothelial Function in Hypertensive Patients

The aim of the study was to evaluate the effect of losartan therapy on endothelial function by measuring serum nitric oxide (NO) levels and urinary excretion of NO in patients with essential hypertension. A group of 30 untreated stage 2 hypertensive patients (15 males and 15 females; age, 51.3 ± 1.5 years) were included in the study. Office systolic and diastolic blood pressure (BP) was measured by using a mercury sphygmomanometer according to phase I and V of Korotkoff sounds. NO levels in serum and 24-hour urine were determined at baseline and after 6 weeks of daily dosing with losartan (50-100 mg). Losartan therapy resulted in a significant fall in systolic/diastolic BP (from 169.7 ± 4.1/105 ± 1.8 mm Hg at baseline to 146 ± 2.7/91 ± 1.9 mm Hg at the end of losartan treatment; P < 0.001). The therapy also caused significant increases in both serum NO level (32.74 ± 3.01 μM/L at baseline versus 79.04 ± 5.17 μM/L; P < 0.001 after therapy) and urinary NO excretion (58.21 ± 3.72 μM/L at baseline versus 113.21 ± 8.63 μM/L; P < 0.001 after therapy). Losartan therapy also reduced serum malondialdehyde (MDA), which is a measure of oxidative stress, by 0.201 nM (15.3%; P = 0.009). Losartan at a dose of 50 to 100 mg per day was effective in reducing elevated BP. The increase in serum NO levels and urinary NO excretion and a decrease in serum MDA levels by losartan treatment indicate a reduction in oxidative stress and enhances NO availability, both of which improve endothelial function. Thus, losartan therapy improves endothelial function in hypertensive patients with essential hypertension.