Cognitive versatility and adaptation to fluid participation in hospital emergency department teams.

Role-based frameworks have long been the cornerstone of organizational coordination, providing clarity in role expectations among team members. However, the rise of "fluid participation"-a constant shift in team composition and skill sets-poses new challenges to traditional coordination mechanisms. In particular, with fluid participation, a team's roles can oscillate between disconnected and intersecting, or between lacking and having overlap in the capabilities and expectations of different roles. This study investigates the possibility that a disconnected set of roles creates a structural constraint on the flexible coordination needed to perform in volatile contexts, as well as the mitigating role of cognitive versatility in a team's strategically-central member. Utilizing a sample of 342 teams from a hospital Emergency Department, we find that teams with a disconnected role set are less effective than teams with an intersecting role set as demonstrated by longer patient stays and increased handoffs during shift changes. Importantly, the presence of a cognitively versatile attending physician mitigates these negative outcomes, enhancing overall team effectiveness. Our findings remain robust even after accounting for other variables like team expertise and familiarity. This research extends the Carnegie School's seminal work on fluid participation by integrating insights from psychology and organizational behavior, thereby identifying key individual attributes that can bolster team coordination in dynamic settings.

Biphasic dyslipidemia in a patient with painless thyroiditis.

In this case study, we followed the thyroid function and serum lipid levels of a patient with painless thyroiditis. Serum lipid levels were decreased during the hyperthyroid phase and elevated during the hypothyroid phase. Both serum lipid levels and thyroid function returned to normative values following a course of thyroid replacement treatment.

Severe hypertriglyceridemia in Japan: Differences in causes and therapeutic responses.

BACKGROUND: Severe hypertriglyceridemia (>1000 mg/dL) has a variety of causes and frequently leads to life-threating acute pancreatitis. However, the origins of this disorder are unclear for many patients. OBJECTIVE: We aimed to characterize the causes of and responses to therapy in rare cases of severe hypertriglyceridemia in a group of Japanese patients. METHODS: We enrolled 121 patients from a series of case studies that spanned 30 years. Subjects were divided into 3 groups: (1) primary (genetic causes); (2) secondary (acquired); and (3) disorders of uncertain causes. In the last group, we focused on 3 possible risks factors for hypertriglyceridemia: obesity, diabetes mellitus, and heavy alcohol intake. RESULTS: Group A (n = 20) included 13 patients with familial lipoprotein lipase deficiency, 3 patients with apolipoprotein CII deficiency, and other genetic disorders in the rest of the group. Group B patients (n = 15) had various metabolic and endocrine diseases. In Group C (uncertain causes; n = 86), there was conspicuous gender imbalance (79 males, 3 females) and most male subjects were heavy alcohol drinkers. In addition, 18 of 105 adult patients (17%) had histories of acute pancreatitis. CONCLUSION: The cause of severe hypertriglyceridemia is uncertain in many patients. In primary genetic forms of severe hypertriglyceridemia, genetic diversity between populations is unknown. In the acquired forms, we found fewer cases of estrogen-induced hypertriglyceridemia than in Western countries. In our clinical experience, the cause of most hypertriglyceridemia is uncertain. Our work suggests that genetic factors for plasma triglyceride sensitivity to alcohol should be explored.

Data from a pre-publication independent replication initiative examining ten moral judgement effects.

We present the data from a crowdsourced project seeking to replicate findings in independent laboratories before (rather than after) they are published. In this Pre-Publication Independent Replication (PPIR) initiative, 25 research groups attempted to replicate 10 moral judgment effects from a single laboratory's research pipeline of unpublished findings. The 10 effects were investigated using online/lab surveys containing psychological manipulations (vignettes) followed by questionnaires. Results revealed a mix of reliable, unreliable, and culturally moderated findings. Unlike any previous replication project, this dataset includes the data from not only the replications but also from the original studies, creating a unique corpus that researchers can use to better understand reproducibility and irreproducibility in science.

Molecular and clinical delineation of 12 patients with glycogen storage disease type III in Western Turkey.

BACKGROUND: Glycogen storage disease type III (GSD III; MIM #232400) is an autosomal recessive inherited disorder characterized by fasting hypoglycemia, growth retardation, hepatomegaly, progressive myopathy, and cardiomyopathy. GSD III is caused by deficiency in the glycogen debranching enzyme (gene symbol: AGL). Molecular analyses of AGL have indicated heterogeneity depending on ethnic groups. In Turkey we reported 13 different AGL mutations from GSD III patients in the Eastern region; however, the full spectrum of AGL mutations in Turkish population remains unclear. Here we investigated 12 GSD III patients mostly from Western Turkey. METHODS: The full coding exons, their relevant exon-intron boundaries, and the 5'- and 3'-flanking regions of the patients' AGL were sequenced. AGL haplotypes were determined. Splicing mutations were characterized by RNA transcript analysis. RESULTS: Twelve different mutations were identified: 7 novel AGL mutations [69-base pair deletion (c.1056_1082+42del69), 21-base par deletion (c.3940_3949+11del21), two small duplications (c.364_365dupCT and c.1497_1500dupAGAG), and 3 splicing mutations (c.1736-11A>G, c.3259+1G>A and c.3588+2T>G)], along with 5 known mutations (c.1019delA, c.958+1G>A, c.4161+5G>A, p.R864X and p.R1218X). Transcripts of splicing mutations (c.1736-11A>G, c.3588+2T>G and c.4161+5G>A) were shown to cause aberrant splicing. AGL haplotype analyses suggested that c.1019delA and c.958+1G>A are founder mutations in Turkish patients, while p.R864X is a recurrent mutation. CONCLUSIONS: Our study broadens the spectrum of AGL mutations and demonstrates that mutations in Western Turkey are different from those in the Eastern region.

Apolipoprotein C-II Tuzla: a novel large deletion in APOC2 caused by Alu-Alu homologous recombination in an infant with apolipoprotein C-II deficiency.

BACKGROUNDS: Familial apolipoprotein (apo) C-II deficiency is a very rare inherited disorder characterized by chylomicronemia. Since the discovery in 1978, reports on apo C-II deficient patients have been limited and only 13 different mutations in APOC2, a gene encoding apo C-II protein, were identified. OBJECTIVES: The objective is to investigate the biochemical and genetic features of a 3-month-old Bosniak girl with chylomicronemia whose apo C-II protein was undetectable in her plasma. METHODS: APOC2, LPL, APOA5, and GPIHBP1 were sequenced. Isoelectrofocusing and immunoblotting of chylomicrons and VLDL fraction from the patient were performed. RESULTS: Sequence analysis demonstrated a large deletion of 2978 base pairs in APOC2, which encompassed exons 2, 3, and 4. The patient was homozygous for the deletion. The 5' part of the breakpoint was located in an Alu Sx repetitive element in intron 1 of APOC2, whereas the 3' part of the breakpoint was in another Alu Sx between APOC2 and CLPTM1, a gene flanking APOC2. We speculate that the deletion was caused by a homologous recombination between two Alu Sx elements. No mutations were detected in LPL, APOA5, and GPIHBP1. Isoelectrofocusing and immunoblotting confirmed the absence of apo C-II protein. CONCLUSIONS: We diagnosed the patient as having apo C-II deficiency and designated the novel large deletion as apo C-II Tuzla. This is the first description of apo C-II deficiency caused by Alu-Alu recombination in APOC2.

The dendrites of granule cell layer neurons are the primary injury sites in the "Brain Diabetes" rat.

We previously demonstrated that rats that receive dorsal third ventricle (3V) streptozotocin (STZ) injections (STZ-3V-rats) exhibit cognitive decline as measured by the Morris Water Maze (MWM) and can be used as an animal model of Alzheimer's disease (AD). Immunohistochemical studies of the hippocampal formations of these animals have revealed significant changes in cerebral insulin signalling pathways, as well as marked increases of amyloid beta (Ab) deposition. Here, we performed Sholl analyses of granule cell layer dendrites and measured dendrite spine densities to assess the effect of STZ on hippocampal morphology. In STZ-3V rats as the results, more branching, complex dendrite arborisation, and increased soma size of the granule cells were observed, while spine densities were decreased in all three spine types. An intraventricular injection of a long-acting insulin analogue improved STZ-induced behavioural and immunohistochemical changes. Nevertheless, dendrite spine densities remained diminished, presumably due to overall null changes since new spine formation due to insulin stimulation has been compensated by loss of old spines. It is concluded that cognitive decline in the "Brain Diabetes" rats is primarily due to impaired intracerebral insulin signalling and the ultimate results were injured excitatory inputs through the perforant pathway.

Lipoprotein lipase activity in heterozygotes for lipoprotein lipase gene mutations reveals a gender bias.

BACKGROUND: Familial lipoprotein lipase (LPL) deficiency is a very rare autosomal recessive disorder characterized by marked elevation of plasma triglyceride concentrations. Since 1989, a variety of mutations have been reported in affected patients. Studies on subjects with heterozygous LPL deficiency, on the other hand, have been limited. METHODS: We examined post-heparin plasma LPL activity in 15 subjects with heterozygous LPL deficiency. RESULTS: The heterozygotes exhibited normal or slightly elevated plasma triglyceride concentrations. The mean LPL activity was reduced by 25% in the heterozygotes relative to controls. Interestingly, LPL activity was reduced specifically in female heterozygotes. CONCLUSION: LPL activity is decreased in female, but not in male, subjects heterozygous for a number of different LPL gene mutations.

Liver cirrhosis treated by living donor liver transplantation in a patient with AGL mutation c.2607-2610delATTC and c.1672dupA.

Glycogen storage disease type III (GSD III) is an inherited disorder characterized by the accumulation of abnormal glycogen in the liver. Hepatic manifestations were considered as improving with age; however, patients live longer and liver cirrhosis is being recognized. We report a patient of GSD IIIa with liver cirrhosis, which was treated successfully by living donor liver transplantation. The patient proved to be a compound heterozygote for a novel small deletion c.2607-2610delATTC and a known duplication c.1672dupA in AGL, a gene coding glycogen debranching enzyme responsible for GSD III. Molecular diagnosis helped clinical decision-making.

Intracerebroventricular administration of an insulin analogue recovers STZ-induced cognitive decline in rats.

We previously demonstrated that intracerebroventricular streptozotocin (STZ-icv) injection induced cognitive dysfunction and led to decreased expression levels of phospho-cyclic AMP responsive element binding protein (pCREB), Akt, and insulin degrading enzyme (IDE) and increased amyloid beta (Ab) deposition in the hippocampus. In the present study, we aimed to investigate whether treatment with an insulin analogue could prevent STZ-induced cognitive decline by reducing or eliminating these changes in the hippocampus. To test this hypothesis, we administrated a long-acting insulin analogue, detemir, into the third ventricle (3V) of STZ-treated rats and assessed cognitive outcomes using the Morris water maze (MWM), immunohistochemistry, and Golgi-Cox staining. Insulin injection successfully rescued STZ-induced cognitive decline, as evidenced by a marked elevation in learning ability. Detemir treatment also resulted in changes in hippocampal levels of IDE, insulin receptor (IR), Akt, somatostatin (SST), and Ab. The STZ-induced decrease of granule cell layer neurons was also recovered by detemir administration. These results provide evidence that 'brain diabetes' and Alzheimer-type dementia involve similar mechanisms and show that insulin may be a promising therapeutic agent to attenuate cognitive decline.

Hepatic lipase activity is decreased in Japanese patients with type III hyperlipoproteinemia.

BACKGROUND: Type III hyperlipoproteinemia (HLP), a disorder associated with a high incidence of premature cardiovascular diseases, is characterized by the accumulation of remnant lipoproteins in the plasma. The primary genetic defect in patients with type III HLP is the presence of apolipoprotein E2 (apoE2), an isoform of apoE, and accumulation of remnant lipoproteins in the plasma has been thought to be attributable to the presence of apoE2, which bind poorly to low density lipoprotein receptors, resulting in defective remnant lipoprotein clearance. On the other hand, the activity of hepatic lipase (HL), the enzyme that plays a pivotal role in the removal of remnant lipoproteins, in type III HLP has not been investigated. METHODS: We examined post-heparin plasma lipoprotein lipase (LPL) and HL activities in 7 patients with type III HLP. The activities of HL and LPL in post-heparin plasma were measured separately by an immunochemical method using antiserum specifically directed against HL. RESULTS: The post-heparin plasma HL activity was significantly reduced, while the LPL activity was normal. CONCLUSIONS: Reduced HL activity may account, at least in part, for the accumulation of remnant lipoproteins in the plasma, a characteristic feature of type III HLP.

Significant reduction of elevated serum lipoprotein(a) concentrations during levo-thyroxine-replacement therapy in a hypothyroid patient.

In a number of previous studies investigators have reported the effect of the thyroid status on the changes of the serum lipoprotein concentrations, whereas reports on serum Lp(a) concentrations have been limited and the results are controversial. Recently, we encountered a hypothyroid patient with elevated serum Lp(a) concentrations in whom serial measurements of serum Lp(a) concentration were performed during the hormone replacement therapy. Our observation on this patient is of particular interest: the serum Lp(a) concentrations tended to continue to decrease even after 1 year 5 months, suggesting that the effects of thyroid hormone on the serum Lp(a) levels may continue for much longer than those on the serum LDL-C. Our findings may suggest a possible role of this hormone in the regulation of Lp(a) metabolism. Together with the recent reports indicating that a thyroid hormone analogue lowered serum Lp(a) levels, our observation may also pave the way for the development of Lp(a)-lowering agents.

Cognitive decline in STZ-3V rats is largely due to dysfunctional insulin signalling through the dentate gyrus.

Recent epidemiological studies have associated type 2 diabetes mellitus with an increased risk of developing Alzheimer's disease (AD). A dramatic decrease in glucose utilisation has been observed in the brains of AD patients, and this decrease has led to the hypothesis that the cognitive dysfunction in AD is associated with decreased central glucose metabolism [1], in addition to cholinergic deficit and elevated amyloid accumulation in the brain [2]. The aims of the present study were to examine the effects of intracerebral administration of streptozotocin (STZ) on cognitive performance in rats as observed by Morris water maze (MWM) task and to clarify the successive insulin-related neurochemical changes through immunohistochemical analysis of the hippocampus. Significant differences were observed in all the parameters of the MWM task (escape latency, path efficiency, average swimming speed and swim path) between STZ-3V-treated and control rats. Immunohistochemical analysis using hippocampal formations revealed significant decreases in phospho-cyclic AMP binding protein, Akt and insulin-degrading enzyme immunoreactivities and a significant increase in amyloid beta immunoreactivity. Our behavioural experiments confirmed that intraventricular administration of STZ led to cognitive impairment, which was ascertained by the changes in hippocampal immunohistochemical markers. In conclusion, we demonstrated that cognitive decline in diabetes was primarily due to impaired intracerebral insulin signalling in addition to arteriosclerotic cerebrovascular changes, which hitherto have been advocated as the main cause of diabetic dementia.

Both eating till feeling full and rapid eating are associated with clustering of psychosomatic problems and preference for strong tastes.

BACKGROUND: Both eating till feeling full and eating rapidly may increase metabolic risk factors including obesity. The associations of such habits with psychosomatic problems and preference for strong tastes require further exploration. METHODS: The associations between various eating behaviors and 12 psychosomatic problems (mental burden, sleep disorder, tendency to palpitation, diarrhea, pessimism, amnesia, anger, poor personal relationship, fatigue, epigastric distress, shoulder stiffness, and lumbago), and preference for strong tastes were compared in 8240 men and 2955 women who underwent routine health examinations. The subjects were divided into four groups defined by subjective reporting - G1: not eating till feeling full and not eating rapidly; G2: eating till feeling full only; G3: eating rapidly only; G4: eating both rapidly and till feeling full. RESULTS: Compared to G1, the age-adjusted odds ratios were significantly higher in G2-G4 for mental burden [1.17 (1.01-1.35), 1.26 (1.14-1.41), 1.50 (1.31-1.73) in men; and 1.28 (1.003-1.62), 1.50 (1.21-1.85), 1.94 (1.50-2.51) in women], and for 8, 8, 11 items in men and 9, 6, 11 items in women among 11 psychosomatic problems other than mental burden, and for preference for strong tastes [2.25 (1.91-2.64), 1.89 (1.67-2.14), 3.36 (2.89-3.91) in men; and 3.26 (2.34-4.51), 2.88 (2.10-3.93), 5.59 (4.02-7.78) in women]. CONCLUSIONS: Both eating till feeling full and eating rapidly are associated with mental burden, clustering of psychosomatic problems and a preference for strong tastes. Mental consultation and attention to choosing mild tasting foods may alleviate such eating behaviors and improve health.

Association of short sleep duration with obesity, diabetes, fatty liver and behavioral factors in Japanese men.

OBJECTIVE: Sleep is one of the major means to maintain health. The association of short sleep duration with obesity, diabetes, fatty liver and behavioral factors requires further exploration. METHODS: A total of 8157 Japanese men who underwent health evaluations were divided into 3 groups by sleep duration <5 hours, 5~<7 hours and ≥7 hours. Poor sleep was self-reported, being defined as difficulty of getting to sleep or awakening easily. The age-adjusted and age and poor sleep-adjusted odds ratios of the 3 groups for obesity, diabetes, fatty liver, mental stress, poor sleep, regular exercise and late dinner time were investigated. RESULTS: Compared to the sleep duration 5~<7 hours group, the age-adjusted odds ratios of the <5 hours group were significantly higher for obesity (1.42), diabetes (1.63), mental stress (1.75), poor sleep (1.85), late dinner time (1.47), and significantly lower for regular exercise (0.61); while those of the ≥7 hours group were significantly lower for obesity (0.73), fatty liver (0.82), mental stress (0.73), poor sleep (0.69), late dinner time (0.45), and significantly higher for regular exercise (1.27). Above significances still existed after adjustment for age and poor sleep. CONCLUSION: Short sleep duration is associated with obesity, diabetes, fatty liver and multiple behavioral factors. The optimal sleep duration for health promotion and effective actions for obtaining optimal sleep, including modifications of behavioral and environmental factors, should be one of the major concerns of public health.

Suppression of the pancreatic duodenal homeodomain transcription factor-1 (Pdx-1) promoter by sterol regulatory element-binding protein-1c (SREBP-1c).

Overexpression of sterol regulatory element-binding protein-1c (SREBP-1c) in ß cells causes impaired insulin secretion and ß cell dysfunction associated with diminished pancreatic duodenal homeodomain transcription factor-1 (PDX-1) expression in vitro and in vivo. To identify the molecular mechanism responsible for this effect, the mouse Pdx-1 gene promoter (2.7 kb) was analyzed in ß cell and non-ß cell lines. Despite no apparent sterol regulatory element-binding protein-binding sites, the Pdx-1 promoter was suppressed by SREBP-1c in ß cells in a dose-dependent manner. PDX-1 activated its own promoter. The E-box (-104/-99 bp) in the proximal region, occupied by ubiquitously expressed upstream stimulatory factors (USFs), was crucial for the PDX-1-positive autoregulatory loop through direct PDX-1·USF binding. This positive feedback activation was a prerequisite for SREBP-1c suppression of the promoter in non-ß cells. SREBP-1c and PDX-1 directly interact through basic helix-loop-helix and homeobox domains, respectively. This robust SREBP-1c·PDX-1 complex interferes with PDX-1·USF formation and inhibits the recruitment of PDX-1 coactivators. SREBP-1c also inhibits PDX-1 binding to the previously described PDX-1-binding site (-2721/-2646 bp) in the distal enhancer region of the Pdx-1 promoter. Endogenous up-regulation of SREBP-1c in INS-1 cells through the activation of liver X receptor and retinoid X receptor by 9-cis-retinoic acid and 22-hydroxycholesterol inhibited PDX-1 mRNA and protein expression. Conversely, SREBP-1c RNAi restored Pdx-1 mRNA and protein levels. Through these multiple mechanisms, SREBP-1c, when induced in a lipotoxic state, repressed PDX-1 expression contributing to the inhibition of insulin expression and ß cell dysfunction.

Lipoprotein(a)-cholesterol: a significant component of serum cholesterol.

BACKGROUND: Lipoprotein(a) [Lp(a)] is known to be a cholesterol-rich lipoprotein, however, the contribution of Lp(a)-cholesterol [Lp(a)-C] to the serum cholesterol and LDL-C levels has not yet been fully evaluated. METHODS: We determined the serum Lp(a)-C in 55 subjects with serum Lp(a) concentrations ranging from 9 to 129 mg/dl. To measure the serum Lp(a)-C concentrations, we developed an immunoaffinity gel assay; serum was incubated with Sepharose 4B gel coupled with immunoglobulin G (IgG) prepared from a polyclonal anti-Lp(a) goat antiserum. After separating Lp(a) from other lipoproteins, we determined the serum Lp(a)-C concentrations. Validation of the assay showed satisfactory results in terms of the specificity and reproducibility. RESULTS: The mean cholesterol content of Lp(a), determined as Lp(a)-C/Lp(a), was 29.5±10.4%. The serum Lp(a)-C values were found to be highly correlated with the serum Lp(a) mass (r=0.923, p<0.001). At serum Lp(a) levels of over 50mg/dl, the contribution of Lp(a)-C to the serum total cholesterol was 10.2%. Further, the Friedewald formula overestimated the serum LDL-C by 20.4%. CONCLUSIONS: Lp(a) contains approximately 30% cholesterol in each molecule. In subjects with markedly elevated serum Lp(a) concentrations, the Lp(a)-C values should be taken into account when evaluating the serum LDL-C.

Eating until feeling full and rapid eating both increase metabolic risk factors in Japanese men and women.

OBJECTIVE: To investigate the association between eating behaviour and metabolic risk in the broader population. DESIGN: The association between metabolic risk factors (overweight, hypertension, hyperglycaemia, hypertriacylglycerolaemia, low HDL cholesterol, hyperuricaemia and fatty liver) and various eating behaviours were compared for four groups defined by subjective reporting: not eating until feeling full and not eating rapidly (G1); eating until feeling full only (G2); eating rapidly only (G3); and eating both rapidly and until feeling full (G4). SETTING: A medical centre for health examinations in Tokyo, Japan. SUBJECTS: Men (n 8240) and women (n 2955) who underwent health examinations. RESULTS: The distribution of participants in G1 to G4 was 49·8 %, 11·5 %, 26·3 % and 12·4 % among men and 55·3 %, 15·0 %, 19·0 % and 10·7 % among women, respectively. Compared with G1, the age-adjusted OR (95 % CI) for overweight were significantly higher in G2 to G4, being respectively 1·85 (1·58, 2·17), 1·98 (1·76, 2·23) and 3·46 (2·99, 4·01) for men and 2·20 (1·62, 2·97), 2·59 (1·97, 3·39) and 3·12 (2·27, 4·26) for women. The age-adjusted OR were also significantly higher for hypertriacylglycerolaemia, hyperuricaemia and fatty liver in G2 and for all risks in G3 and G4 among men; and for hyperuricaemia in G2, for hyperglycaemia, hypertriacylglycerolaemia and fatty liver in G3 and for hypertriacylglycerolaemia and fatty liver in G4 among women. CONCLUSIONS: Both eating until feeling full and eating rapidly increase metabolic risk factors. Although the mechanism between rapid eating and metabolic risk requires further exploration, eating slowly and ending meals shortly before feeling full are important public health messages for reducing metabolic risk factors.

Non-HDL-cholesterol/apolipoprotein B ratio: a useful distinguishing feature in the screening for type III hyperlipoproteinemia.

BACKGROUND: Dysbetalipoproteinemia, also known as type III hyperlipoproteinemia (type III HL), is characterized by the accumulation of ß-very low density lipoprotein (ß-VLDL). However, demonstration of the presence of ß-VLDL is not easy because it requires preparative ultracentrifugation of lipoproteins. The primary genetic defect in type III HL is the presence of apolipoprotein (apo) E2, a mutant form of apoE. However, another metabolic defect, such as overproduction of VLDL, is also required for the full phenotype. Patients with only E2 homozygosity usually do not have HL. Because apoE genotyping is expensive, the selection of patients for this analysis by effective use of common clinical measures would be very helpful. OBJECTIVE: We examined the non-HDL-C/apoB ratio as an index for type III HL screening. METHODS: We studied nine patients with type III HL. Most patients with type III HL show mixed hyperlipidemia. We compared the plasma of patients with combined hyperlipidemia and the dyslipidemia of hypothyroidism with those with type III HL. The serum levels of total cholesterol, triglyceride, and high-density lipoprotein cholesterol (HDL-C), as well as the serum apoB and apoE levels, were measured by routine laboratory methods. RESULTS: Individual values of serum lipids and apolipoproteins did not distinguish type III HL from the two other types of HL. The non-HDL-C/apoB ratio in type III HL was significantly greater than that in the two comparison groups, with no overlap. CONCLUSION: The non-HDL-C/apoB ratio is a novel index that appears to be reliable for screening of patients for type III HL, and the index can be determined at regular clinical laboratories without the need for any complicated lipoprotein analysis. Thus, we propose the clinical usefulness of this index.