PELAKSANAAN PEMBERIAN KREDIT BANK BERDASARKAN UNDANG-UNDANG NOMOR 10 TAHUN 1998

Tujuan dilakukannya penelitian ini adalah untuk mengetahui bagaimana proses pelaksanaan pemberian kredit oleh bank kepada nasabah dan apa saja jenis-jenis kredit yang diberikan bank kepada nasabah, di mana dengan menggunakan metode penelitian hukum normatif disimpulkan: 1. Proses pelaksanaan pemberian kredit oleh bank kepada nasabah merupakan suatu proses yang harus dilewati nasabah untuk mendapatkan fasilitas kredit yang diinginkan. Adapun prosesnya pelaksanaannya yaitu pengajuan permohonan kredit, penyidikan dan analisis kredit, keputusan kredit, pelolakan kredit, persetujuan kredit yang didalamnya meliputi kegiatan pengikatan jaminan kredit dan penandatangan perjanjian kredit, dan terakhir adalah pencairan kredit. Pencairan kredit dilaksanakan sebagaimana disepakati dalam perjanjian kredit yang telah dibuat. 2. Jenis-jenis pemberian kredit bank kepada nasabahnya yaitu kredit yang diberikan Bank Indonesia dan kredit yang diberikan bank kepada masyarakat. Kredit yang diberikan Bank Indonesia meliputi kredit langsung, kredit investasi dan fasilitas diskonto. Berikutnya kredit yang diberikan perbankan kepada masyarakat yaitu jenis kredit berdasarkan penggunaan kredit meliputi kredit modal kerja dan investasi, jenis kredit berdasarkan tujuan kredit meliputi kredit produktif, kredit konsumtif, dan jenis kredit perdagangan, jenis kredit berdasarkan jangka waktu kredit meliputi kredit jangka pendek (Short Term Loan), kredit jangka menengah (Medium Term Loan) dan kredit jangka panjang (long Term Loan).Kata kunci:  bank; kredit

Global Gene Expression Analysis in the Livers of Rat Offspring Perinatally Exposed to Low Doses of 2,2′,4,4′-Tetrabromodiphenyl Ether

BACKGROUND: Polybrominated diphenyl ethers are a group of flame-retardant chemicals appearing increasingly in the environment. Their health effects and mechanisms of toxicity are poorly understood. OBJECTIVES: We screened for the sensitive effects and mechanisms of toxicity of 2,2 ,4,4 -tetra-bromodiphenyl ether (BDE-47) by analyzing the gene expression profile in rats exposed to doses comparable to human exposure. METHODS: Wistar dams were exposed to vehicle or BDE-47 (0.002 and 0.2 mg/kg body weight) every fifth day from gestation day 15 to postnatal day 20 by injections to caudal vein. Total RNA was extracted from the livers of pups and hybridized to the whole-genome RNA expression micro-arrays. The list of genes 2-fold differentially expressed was exported to PANTHER and Ingenuity Systems for analysis of enriched ontology groups and molecular pathways. RESULTS: Oxidoreductase and transferase protein families were enriched in exposed rats as were these biological process categories: carbohydrate metabolism; electron transport; and lipid, fatty acid, and steroid metabolism. Four signaling pathways (cascades of activation of drug-metabolizing enzymes) and 10 metabolic pathways were significantly enriched. Drug-metabolizing enzymes appear to be regulated by BDE-47 through an aryl hydrocarbon receptor-independent mechanism. Direct interaction with retinoid X receptor or its upstream cascade may be involved. The main metabolic effects consisted of activation of metabolic pathways: alpha- and omega-oxidation of fatty acids, glycolysis, and starch hydrolysis. CONCLUSIONS: Altered expression of genes involved in metabolic and signaling pathways and functions of the organism occurs after perinatal exposure of rat offspring to BDE-47 at doses relevant for the general population

Heavy Metal Hazards of Pediatric Syrup Administration in Nigeria: A Look at Chromium, Nickel and Manganese

Fifty different pediatric syrups were randomly sampled from patent medicine stores and pharmaceutical shops within Awka (Anambra State, Nigeria) between November 2007 and May 2008. Syrups were ashed before digestion using conc. aqua regia, HCl: HNO3 (3:1). Chromium, nickel and manganese were assayed with AAS 205A. The highest levels of nickel were seen in Magcid suspension (4.13 mg/L) and Gaviron (0.79 mg/L) whereas lowest levels were found in Asco–J vitamin and Jawaron Syrup (0.01 mg/L). About 44.1, 73.6 and 20.6% of the sampled syrups made in Nigeria had non detectable levels of nickel, chromium and manganese respectively. Chromium levels ranged from 0.01 mg/L in Magcid suspension to 0.58 mg/L in emvite. Ferobin and Jawaron Syrup plus had 28.23 and 4.37 mg/L manganese, respectively. With the exception of Cephalexin Syrup, all the imported syrups had non detectable levels of chromium. The level of chromium in Cephalexin Syrup was 0.01 mg/L. About 68.8 and 43.7% of these imported syrups had non-detectable levels of nickel and manganese respectively. Nickel levels ranged from 0.01–0.09 mg/L in the imported syrups. Haemoglobin Syrup showed highest level of manganese of 0.36 mg/L whereas the lowest concentration was 0.02 mg/L in Cadiphen. Taken together the Nigerian made syrup samples had higher concentrations of the studied heavy metals. It is feared that ingestion of these syrups may constitute a significant source of heavy metal exposure to the children and should therefore be considered a public health problem. The public health hazards from ingestion of these syrups should be identified and disclosed by in-depth risk assessment studies

Thyroid Hormones in Pregnancy in Relation to Environmental Exposure to Organochlorine Compounds and Mercury

Polychlorinated biphenyls (PCBs), chlorinated pesticides, and mercury are global environmental contaminants that can disrupt the endocrine system in animals and humans. However, there is little evidence that they can interfere with endocrine status in pregnant women and neonates at low levels of exposure. The aim of this study was to examine thyroid hormone levels during pregnancy and in cord blood in relation to blood concentrations of organochlorine compounds (OCs) and Hg in healthy women recruited during pregnancy. We found a significant negative correlation between maternal total triiodothyronine levels and three non-coplanar congeners (PCB-138, PCB-153, and PCB-180), three pesticides (p,p′-DDE, cis-nanochlor, and hexachlorobenzene), and inorganic Hg independently, without any other changes in thyroid status. No significant relationships were observed between OCs and cord serum thyroid hormones. Cord serum free thyroxin was negatively correlated with inorganic Hg. These results suggest that at even low levels of exposure, persistent environmental contaminants can interfere with thyroid status during pregnancy

In Utero Exposure to Persistent Organic Pollutants and Childhood Lipid Levels

Animal studies have shown that developmental exposures to polybrominated diphenyl ethers (PBDE) permanently affect blood/liver balance of lipids. No human study has evaluated associations between in utero exposures to persistent organic pollutants (POPs) and later life lipid metabolism. In this pilot, maternal plasma levels of PBDEs (BDE-47, BDE-99, BDE-100, and BDE-153) and polychlorinated biphenyls (PCB-138, PCB-153, and PCB-180) were determined at delivery in participants of GESTation and Environment (GESTE) cohort. Total cholesterol (TCh), triglycerides (TG), low- and high-density lipoproteins (LDL-C and HDL-C), total lipids (TL), and PBDEs were determined in serum of 147 children at ages 6–7. General linear regression was used to estimate the relationship between maternal POPs and child lipid levels with adjustment for potential confounders, and adjustment for childhood POPs. In utero BDE-99 was associated with lower childhood levels of TG (p = 0.003), and non-significantly with HDL-C (p = 0.06) and TL (p = 0.07). Maternal PCB-138 was associated with lower childhood levels of TG (p = 0.04), LDL-C (p = 0.04), and TL (p = 0.02). Our data indicate that in utero exposures to POPs may be associated with long lasting decrease in circulating lipids in children, suggesting increased lipid accumulation in the liver, a mechanism involved in NAFLD development, consistent with previously reported animal data

Establishing non-fasting reference values for plasma lipids levels based on age, sex, and puberty stage in a French-Canadian pediatric population

Background Dyslipidemias, including familial hypercholesterolemia (FH), are a significant risk factor for cardiovascular diseases. FH is a genetic disorder resulting in elevated levels of low-density lipoprotein cholesterol (LDL-C) and an increased probability of early cardiovascular disorders. Heterozygous familial hypercholesterolemia (HeFH) is the most common form, affecting approximately 1 in 250 individuals worldwide, with a higher prevalence among the French-Canadian population. Childhood is a critical period for screening risk factors, but the recommendation for non-fasting screening remains controversial due to a lack of specific reference values for this state. This study aims to establish reference values for lipid levels in non-fasting children from Sherbrooke, Quebec, Canada, that will be specific for sex, age, and pubertal stages. Methods Blood samples and corresponding anthropometric data were collected from 356 healthy children aged from 6 to 13. They were categorized either into two age groups: Cohort 6–8 and Cohort 9–13, or into pubertal stages. Reference values, specifically the 2.5th, 5th, 10th, 50th, 90th, 95th, and 97.5th percentiles were determined using the CLSI C28-A3 guidelines. Results Lipid profiles did not significantly differ between sexes, except for higher levels of high-density lipoprotein (HDL-C) in boys within Cohort 6–8. HDL-C levels significantly increased, while LDL-C and non-HDL-C levels significantly decreased in both sexes with age. Non-fasting age- and pubertal stages-specific reference values were established. Conclusion This study established reference intervals for lipid markers in non-fasting state within the pediatric French-Canadian population. These findings could be used in dyslipidemia screening in daily practice

Associations of iron metabolism genes with blood manganese levels: a population-based study with validation data from animal models

<p>Abstract</p> <p>Background</p> <p>Given mounting evidence for adverse effects from excess manganese exposure, it is critical to understand host factors, such as genetics, that affect manganese metabolism.</p> <p>Methods</p> <p>Archived blood samples, collected from 332 Mexican women at delivery, were analyzed for manganese. We evaluated associations of manganese with functional variants in three candidate iron metabolism genes: <it>HFE </it>[hemochromatosis], <it>TF </it>[transferrin], and <it>ALAD </it>[δ-aminolevulinic acid dehydratase]. We used a knockout mouse model to parallel our significant results as a novel method of validating the observed associations between genotype and blood manganese in our epidemiologic data.</p> <p>Results</p> <p>Percentage of participants carrying at least one copy of <it>HFE C282Y</it>, <it>HFE H63D</it>, <it>TF P570S</it>, and <it>ALAD K59N </it>variant alleles was 2.4%, 17.7%, 20.1%, and 6.4%, respectively. Percentage carrying at least one copy of either <it>C282Y </it>or <it>H63D </it>allele in <it>HFE </it>gene was 19.6%. Geometric mean (geometric standard deviation) manganese concentrations were 17.0 (1.5) μg/l. Women with any <it>HFE </it>variant allele had 12% lower blood manganese concentrations than women with no variant alleles (β = -0.12 [95% CI = -0.23 to -0.01]). <it>TF </it>and <it>ALAD </it>variants were not significant predictors of blood manganese. In animal models, <it>Hfe</it>^-/-mice displayed a significant reduction in blood manganese compared with <it>Hfe</it>^+/+mice, replicating the altered manganese metabolism found in our human research.</p> <p>Conclusions</p> <p>Our study suggests that genetic variants in iron metabolism genes may contribute to variability in manganese exposure by affecting manganese absorption, distribution, or excretion. Genetic background may be critical to consider in studies that rely on environmental manganese measurements.</p

Facing the Challenge of Data Transfer from Animal Models to Humans: the Case of Persistent Organohalogens

A well-documented fact for a group of persistent, bioaccumulating organohalogens contaminants, namely polychlorinated biphenyls (PCBs), is that appropriate regulation was delayed, on average, up to 50 years. Some of the delay may be attributed to the fact that the science of toxicology was in its infancy when PCBs were introduced in 1920's. Nevertheless, even following the development of modern toxicology this story repeats itself 45 years later with polybrominated diphenyl ethers (PBDEs) another compound of concern for public health. The question is why? One possible explanation may be the low coherence between experimental studies of toxic effects in animal models and human studies. To explore this further, we reviewed a total of 807 PubMed abstracts and full texts reporting studies of toxic effects of PCB and PBDE in animal models. Our analysis documents that human epidemiological studies of PBDE stand to gain little from animal studies due to the following: 1) the significant delay between the commercialisation of a substance and studies with animal models; 2) experimental exposure levels in animals are several orders of magnitude higher than exposures in the general human population; 3) the limited set of evidence-based endocrine endpoints; 4) the traditional testing sequence (adult animals – neonates – foetuses) postpones investigation of the critical developmental stages; 5) limited number of animal species with human-like toxicokinetics, physiology of development and pregnancy; 6) lack of suitable experimental outcomes for the purpose of epidemiological studies. Our comparison of published PCB and PBDE studies underscore an important shortcoming: history has, unfortunately, repeated itself. Broadening the crosstalk between the various branches of toxicology should therefore accelerate accumulation of data to enable timely and appropriate regulatory action