編集後記

Mengelola operasional bank komersial memerlukan keahlian yang mumpuni di berbagai bidang. Buku ini merupakan buku pertama dari dua buku mengenai pengelolaan bank komersial. Di buku ini dibahas pengelolaan operasional kantor cabang, sedangkan di buku kedua akan dibahas pengelolaan operasional kantor dengan tingkatan yang lebih tinggi. Buku pertama ini ditujukan bagi para calon pimpinan cabang dan para pejabat yang sudah menduduki posisi pimpinan cabang untuk lebih memahami berbagai hal terkait pengelolaan kantor cabang. Disusun oleh Pokja General Banking II Ikatan Bankir Indonesia dan Lembaga Sertifikasi Profesi Perbankan dengan melibatkan berbagai pakar di bida ngnya, buku ini merupakan referensi wajib bagi setiap calon peserta sertifikasi General Banking Tingkat II. Buku ini juga disertai latihan soal yang membantu pembaca memahami isi buku sekaligus mempersiapkan diri mengikuti ujian sertifikasi

Depression and anxiety may be cause or effect of attacks in hereditary angioedema

Introduction: The study aims to determine the depression and anxiety levels of patients with hereditary angioedema using the Beck depression inventory(BDI), Beck anxiety inventory (BAI) and to compare the results with the patients' demographic characteristics, the number of attacks, attack types, and healthy controls.Methods: 60 hereditary angioedema patients and 60 healthy controls were included in the study. The demographic characteristics of the patients, the total number of attacks/months before treatment, the number of attacks according to the localization of the attacks, and the number of attacks/month after treatment were filled in retrospectively from their hospital records. BDI and BAI were used for anxiety and depression levels.Results: Median BAI (11 vs 5; p=0.001) and BDI (11 vs 7; p=0.024) in HAE patients, the ratio of patients with moderate anxiety (21.7% vs 1.7%; p=0.001) and the ratio of patients with severe anxiety (8.3% vs. 0%; p=0.001) were compared to the control group, was high. There was no statistically significant difference between the number of attacks under treatment and the BAI and BDI scores. A positive correlation was found between the number of untreated attacks and the number of attacks under treatment and the BAI score (r=0.759; p=0.001) and BDI score (r=0.599; p=0.001).Conclusions: Due to the high prevalence of depression and anxiety in HAE patients, health care providers should be attentive of this comorbidity and refer patients to mental health specialists, when needed.Keywords: Hereditary Angioedema, Beck Depression Inventory, Beck Anxiety Inventor

UT-B-deficient mice develop renal dysfunction and structural damage

<p>Abstract</p> <p>Background</p> <p>Urea transporter UT-B is the major urea transporter in erythrocytes and the descending vasa recta in the kidney. In this study, we investigated the effects of long-term UT-B deficiency on functional and structural defect in the kidney of 16-and 52-week-old UT-B-null mice.</p> <p>Methods</p> <p>UT-B-knockout mice were generated by targeted gene disruption and lacked UT-B protein expression in all organs. The urinary concentrating ability of mice was studied in terms of daily urine output, urine osmolality, and urine and plasma chemistries. Changes in renal morphology were evaluated by hematoxylin and eosin staining.</p> <p>Results</p> <p>The UT-B-null mice showed defective urine concentrating ability. The daily urine output in UT-B-null mice (2.5 ± 0.1 ml) was 60% higher and urine osmolality (985 ± 151 mosm) was significantly lower than that in wild-type mice (1463 ± 227 mosm). The 52-week-old UT-B-null mice exhibited polyuria after water deprivation, although urine osmolality was increased. At 52 weeks of age, over 31% of UT-B-null mice exhibited renal medullary atrophy because of severe polyuria and hydronephrosis.</p> <p>Conclusions</p> <p>Long-term UT-B deficiency causes severe renal dysfunction and structural damage. These results demonstrate the important role of UT-B in countercurrent exchange and urine concentration.</p

Utilization of Colemanite waste in Concrete Design

Waste material is formed in enormous quantities during the beneficiation of raw ore. These wastes can cause both economic loss and environmental pollution. Thus, in this study, the effect of CW obtained from Eti Mine Establishments Kütahya-Emet Boron Plants on the compressive strength and cylinder splitting tensile strength of concrete and its USAbility as a concrete admixture is investigated. The results found show that utilization of Colemanite Waste is possible when it is used as additive in concrete

Metabolic changes in summer active and anuric hibernating free-ranging brown bears (ursus arctos)

The brown bear (Ursus arctos) hibernates for 5 to 6 months each winter and during this time ingests no food or water and remains anuric and inactive. Despite these extreme conditions, bears do not develop azotemia and preserve their muscle and bone strength. To date most renal studies have been limited to small numbers of bears, often in captive environments. Sixteen free-ranging bears were darted and had blood drawn both during hibernation in winter and summer. Samples were collected for measurement of creatinine and urea, markers of inflammation, the calcium-phosphate axis, and nutritional parameters including amino acids. In winter the bear serum creatinine increased 2.5 fold despite a 2-fold decrease in urea, indicating a remarkable ability to recycle urea nitrogen during hibernation. During hibernation serum calcium remained constant despite a decrease in serum phosphate and a rise in FGF23 levels. Despite prolonged inactivity and reduced renal function, inflammation does not ensue and bears seem to have enhanced antioxidant defense mechanisms during hibernation. Nutrition parameters showed high fat stores, preserved amino acids and mild hyperglycemia during hibernation. While total, essential, non-essential and branched chain amino acids concentrations do not change during hibernation anorexia, changes in individual amino acids ornithine, citrulline and arginine indicate an active, although reduced urea cycle and nitrogen recycling to proteins. Serum uric acid and serum fructose levels were elevated in summer and changes between seasons were positively correlated. Further studies to understand how bears can prevent the development of uremia despite minimal renal function during hibernation could provide new therapeutic avenues for the treatment of human kidney disease

Validation of Surrogates of Urine Osmolality in Population Studies

The importance of vasopressin and/or urine concentration in various kidney, cardiovascular, and metabolic diseases has been emphasized recently. Due to technical constraints, urine osmolality (Uosm), a direct reflect of urinary concentrating activity, is rarely measured in epidemiologic studies. We analyzed 2 possible surrogates of Uosm in 4 large population-based cohorts (total n = 4,247) and in patients with chronic kidney disease (CKD, n = 146). An estimated Uosm (eUosm) based on the concentrations of sodium, potassium, and urea, and a urine concentrating index (UCI) based on the ratio of creatinine concentrations in urine and plasma were compared to the measured Uosm (mUosm). eUosm is an excellent surrogate of mUosm, with a highly significant linear relationship and values within 5% of mUosm (r = 0.99 or 0.98 in each population cohort). Bland-Altman plots show a good agreement between eUosm and mUosm with mean differences between the 2 variables within ±24 mmol/L. This was verified in men and women, in day and night urine samples, and in CKD patients. The relationship of UCI with mUosm is also significant but is not linear and exhibits more dispersed values. Moreover, the latter index is no longer representative of mUosm in patients with CKD as it declines much more quickly with declining glomerular filtration rate than mUosm. The eUosm is a valid marker of urine concentration in population-based and CKD cohorts. The UCI can provide an estimate of urine concentration when no other measurement is available, but should be used only in subjects with normal renal function

The Urine-to-Plasma Urea Concentration Ratio is associated with eGFR and eGFR decline over time in a population cohort.

BACKGROUND Evaluation of renal function and of factors associated with its decline are important public health issues. Besides markers of glomerular function (e.g., GFR), those of tubular functions are rarely evaluated. Urea, the most abundant urinary solute, is markedly concentrated in urine when compared to plasma. We explored the urine-to-plasma ratio of urea concentrateions (U/P-urea-ratio) as a marker of tubular functions. METHODS We evaluated the relationship of the U/P-urea-ratio with eGFR at baseline in 1043 participants (48±17y) from the SKIPOGH population-based cohort, using mixed regression. In 898 participants, we assessed the relation between U/P-urea-ratio and renal function decline between two study waves 3 years apart. We studied U/P ratios for osmolarity, Na, K, uric acid for comparison. RESULTS In a transversal study at baseline, eGFR was positively associated with U/P-urea-ratio (βscaled = 0.08, 95%CI[0.04;0.13]) but not with the U/P ratio of osmolarity. Considering separately participants with renal function > or ≤ 90 ml/minx1.73m2, this association was observed only in those with reduced renal function. In the longitudinal study, eGFR declined at a mean rate of 1.2 ml/min per year. A significant association was observed between baseline U/P-urea-ratio and eGFR decline (βscaled = 0.08, 95%CI[0.01;0.15]). A lower baseline U/P-urea-ratio was associated with a greater eGFR decline. CONCLUSION This study provides evidence that the U/P-urea-ratio is an early marker of kidney function decline in the general adult population. Urea is easy to measure with well-standardized techniques and at low cost. Thus, the U/P-urea-ratio could become an easily available tubular marker for evaluating renal function decline

Role of the urinary concentrating process in the renal effects of high protein intake

Role of the urinary concentrating process in the renal effects of high protein intake. High protein diet is known to increase glomerular filtration rate (GFR) and induce kidney hypertrophy. The mechanisms underlying these changes are not understood. Since the mammalian kidney comprises different nephron segments located in well-delineated zones, it is conceivable that the hypertrophy does not affect all kidney zones and all nephron segments uniformly. The present experiments were designed to study the chronic effects of high or low isocaloric protein diets (HP = 32% or LP = 10% casein, respectively) on kidney function and morphology in Sprague-Dawley rats. HP diet induced significant increases in kidney mass, GFR, free water clearance, and maximum urine concentrating ability. Kidney hypertrophy was characterized by: 1. a preferential increase in thickness of the inner stripe of the outer medulla (IS) (+ 54%, P < 0.001, while total kidney height, from cortex to papillary tip, increased only by 18%); 2. a marked hypertrophy of the thick ascending limbs (TAL) in the inner stripe (+40% epithelium volume/unit tubular length, P < 0.05) but not in the outer stripe nor in the cortex; 3. an increase in heterogeneity of glomeruli between superficial (S) and deep (D) nephrons (D/S = 1.47 in HP vs. 1.17 in LP, P < 0.05). In contrast, normal kidney growth with age and kidney hypertrophy induced by uninephrectomy were not accompanied by preferential enlargement of IS structures. The morphologic changes induced by high protein intake parallel those we previously reported in rats fed a normal diet (25% protein) but in which the operation of the urine concentrating mechanism was chronically stimulated by ADH infusion or by reduction in water intake. This similarity and the dramatic increase in free water reabsorption induced by HP diet suggest that high protein intake affects kidney function and morphology by increasing the level of operation of the urine concentrating process. The preferential increase in TAL epithelium disclosed in this study, and the recent demonstration by others of a decreased salt concentration in the early distal tubule of HP rats raises the possibility that the protein-induced increase in GFR is mediated by a depression of tubuloglomerular feedback resulting from an increased salt transport in the medullary TAL in relation with an increase in free water generation

Renal and Blood Pressure Response to a High-Salt Diet in Mice With Reduced Global Expression of the Glucocorticoid Receptor

Salt-sensitive hypertension is common in glucocorticoid excess. Glucocorticoid resistance also presents with hypercortisolemia and hypertension but the relationship between salt intake and blood pressure (BP) is not well defined. GRβgeo/+ mice have global glucocorticoid receptor (GR) haploinsufficiency and increased BP. Here we examined the effect of high salt diet on BP, salt excretion and renal blood flow in GRβgeo/+mice. Basal BP was ∼10 mmHg higher in male GRβgeo/+ mice than in GR+/+ littermates. This modest increase was amplified by ∼10 mmHg following a high-salt diet in GRβgeo/+ mice. High salt reduced urinary aldosterone excretion but increased renal mineralocorticoid receptor expression in both genotypes. Corticosterone, and to a lesser extent deoxycorticosterone, excretion was increased in GRβgeo/+ mice following a high-salt challenge, consistent with enhanced 24 h production. GR+/+ mice increased fractional sodium excretion and reduced renal vascular resistance during the high salt challenge, retaining neutral sodium balance. In contrast, sodium excretion and renal vascular resistance did not adapt to high salt in GRβgeo/+ mice, resulting in transient sodium retention and sustained hypertension. With high-salt diet, Slc12a3 and Scnn1a mRNAs were higher in GRβgeo/+ than controls, and this was reflected in an exaggerated natriuretic response to thiazide and benzamil, inhibitors of NCC and ENaC, respectively. Reduction in GR expression causes salt-sensitivity and an adaptive failure of the renal vasculature and tubule, most likely reflecting sustained mineralocorticoid receptor activation. This provides a mechanistic basis to understand the hypertension associated with loss-of-function polymorphisms in GR in the context of habitually high salt intake

Heat acclimatization blunts copeptin responses to hypertonicity from dehydrating exercise in humans.

Acclimatization favors greater extracellular tonicity from lower sweat sodium, yet hyperosmolality may impair thermoregulation during heat stress. Enhanced secretion or action of vasopressin could mitigate this through increased free water retention. Aims were to determine responses of the vasopressin surrogate copeptin to dehydrating exercise and investigate its relationships with tonicity during short and long-term acclimatization. Twenty-three participants completed a structured exercise programme following arrival from a temperate to a hot climate. A Heat Tolerance Test (HTT) was conducted on Day-2, 6, 9 and 23, consisting of 60-min block-stepping at 50% VO2 peak, with no fluid intake. Resting sweat [Na+ ] was measured by iontophoresis. Changes in body mass (sweat loss), core temperature, heart rate, osmolality (serum and urine) and copeptin and aldosterone (plasma) were measured with each Test. From Day 2 to Day 23, sweat [Na+ ] decreased significantly (adjusted P < 0.05) and core temperature and heart rate fell. Over the same interval, HTT-associated excursions were increased for serum osmolality (5 [-1, 9] vs. 9 [5, 12] mosm·kg-1 ), did not differ for copeptin (9.6 [6.0, 15.0] vs. 7.9 [4.3, 14.7] pmol·L-1 ) and were reduced for aldosterone (602 [415, 946] vs. 347 [263, 537] pmol·L-1 ). Urine osmolality was unchanging and related consistently to copeptin at end-exercise, whereas the association between copeptin and serum osmolality was right-shifted (P = 0.0109) with acclimatization. Unchanging urine:serum osmolality argued against increased renal action of vasopressin. In conclusion, where exercise in the heat is performed without fluid replacement, heat acclimatization does not appear to enhance AVP-mediated free water retention in humans