Increase of child car seat temperature in cars parked in the outpatient parking lot

Background: A guideline for the safe use of child car seats (CS) was published by the Japan Pediatric Society in 2008. There have been few studies of the increase of temperature of a CS in parked cars. The aim of this study was to determine the change in the temperature of the CS in cars parked in full sun. Methods: The temperature of CS was measured during summer (July and August) in 2006, 2007, and 2008. The CS used in this study (n= 50) were for children (≤6 years old) who were taken by car to Sugimura Children's Medical Clinic. Temperatures were only measured on sunny days. Measurements were performed from 09.00 to 17.00 hours. Thermochron (Thermochron i‐Button: G type, Maxim Integrated Products, CA, USA) was used to measure the temperatures. The maximum temperatures of CS were compared in time at the clinic, taking into consideration seat colors, and car colors. Results: Of the 50 cars, three cars were excluded due to being in the shade while the temperature was measured. A total of 47 cars were used for this study. The temperature of the CS ranged from 38.0 to 65.5°C (47.8 ± 5.8°C). Eighteen CS (38.3%) reached a temperature of 50°C or above. The maximum temperature of the 13.00?15.00‐hours group was significantly higher than that of the 09.00?11.00‐hours group (P= 0.035). The CS temperatures in the black car group were significantly higher than those of the white car group (P= 0.013). Conclusion: CS may become very hot while a car is parked in sun, especially if the car and the CS are black, so the CS should be cooled before a young child is placed in it. Guardians of small children should be aware of this risk.     

Twenty-six-week oral toxicity of diheptyl phthalate with special emphasis on its induction of liver proliferative lesions in male F344 rats

The 26-week oral toxicity of diheptyl phthalate (DHP), a peroxisome proliferator-activated receptor α (PPARα) agonist, with special emphasis on the potential induction of hepatocellular proliferative lesions was investigated in this study. DHP was administered to male F344 rats via gavage at 0 (control), 1,000 or 2,000 mg/kg/day for 26 weeks. Body weight gain was significantly lower, whereas food and water consumption was significantly higher in DHP-treated rats compared with controls. DHP-treated rats exhibited decreases in blood triglyceride, total cholesterol, phospholipid and glucose levels, which were likely related to biological effects of the PPARα agonist. Absolute and relative organ weights of the livers with pale brown discoloration and dark brown spots significantly increased in DHP-treated rats. Histopathological examinations revealed remarkable diffuse hypertrophy of hepatocytes with ground-glass appearance, intracytoplasmic inclusion bodies and/or vacuolation in the DHP-treated groups. These findings were associated with increases in serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and γ-glutamyltranspeptidase. The number and area of glutathione S-transferase placental form positive foci, a marker of hepatocellular preneoplastic lesions in rats, significantly increased in DHP-treated groups. Additionally, proliferating cell nuclear antigen positive liver cell counts in DHP-treated groups were significantly higher than those of the controls. Testicular alterations were not detected histopathologically, whereas absolute and relative prostate weights significantly decreased at both doses. These results indicate that DHP induces liver pre-neoplastic foci, and suggest the possibility that DHP is a possible genotoxic carcinogen in the liver of rats.     

A pitfall of fractional flow reserve associated with the presence of collateral circulation

An 82-year-old man had a severe stenosis in the proximal left anterior descending artery (LAD) and an intermediate stenosis in the distal right coronary artery (RCA). The territory of mid to distal LAD was perfused via an angiographically well-developed collateral circulation from the distal RCA. Fractional flow reserve (FFR) in the distal RCA was 0.84. After successful coronary intervention for the proximal LAD, repeat FFR in the distal RCA was 0.96. In this case, the severity of the stenosis in the donor artery was overestimated by using FFR due to the presence of well-developed collateral circulation.     

Pioglitazone improves endothelium-dependent vasodilation in hypertensive patients with impaired glucose tolerance in part through a decrease in oxidative stress

Background

The aim of this study was to determine pioglitazone treatment restores endothelial function in hypertensive patients with impaired glucose tolerance (IGT).

Methods and results

We evaluated the effects of pioglitazone treatment for 12 weeks on forearm blood flow (FBF) responses to acetylcholine and sodium nitroprusside in 34 hypertensive patients with IGT who were randomly divided into a pioglitazone group (n = 17) and an amlodipine monotherapy group (n = 17) and in 34 healthy subjects. Pioglitazone, but not amlodipine, increased the FBF response to acetylcholine and decreased urinary excretion of 8-hydroxy-2′-deoxyguanosine. Pioglitazone did not alter sodium nitroprusside-stimulated vasodilation. N^G-monomethyl-l-arginine abolished the augmentation of FBF response to acetylcholine after pioglitazone treatment. The increase in maximal FBF response to acetylcholine correlated with the decrease in urinary excretion of 8-hydroxy-2′-deoxyguanosine.

Conclusion

Pioglitazone improved endothelial function in hypertensive patients with IGT through an increase in nitric oxide bioavailability by, in part, a decrease in oxidative stress.     

Apolipoprotein B and small, dense LDL-C

Apolipoprotein B-100 (apo B-100) and small, dense LDL-C (sdLDL-C) are beneficial risk markers for CHD. Apo B-100 indicates the number of LDL particles that reflect the risk of CHD better than the LDL-C concentration. SdLDL is a lipoprotein subclass that causes arteriosclerosis with a much higher risk than large LDL. Apo B-100 is measured by a fully automated turbidimetric immunoassay, while small-dense LDL-C is measured by an enzymatic homogeneous assay with an automated analyzer. Elevated apo B-100 and sdLDL-C are observed among people with familial hypercholesterolemia, familial combined hyperlipidemia, diabetes mellitus, or metabolic syndrome, all of which lead to CHD with high probability. Although both apo B-100 and sdLDL-C are high in all of these cases, the two markers show noticeably different tendencies for each case. Familial hypercholesterolemia patients have higher apo B-100 than sdLDL-C; in contrast, people with diabetes mellitus or metabolic syndrome have higher sdLDL-C than apo B-100. Familial combined hyperlipidemia cases do not show much difference between the two values. The results of both apo B-100 or sdLDL-C can be good risk markers of CHD when tested individually, whereas the cause of CHD may be further clarified by assessing them in combination. By identifying the cause, patients can receive appropriate medical treatments. In conclusion, measuring both apo B-100 and sd LDL-C potentially implies further additional information on clinical utility.     

Adenosine thiamine triphosphate (AThTP) inhibits poly(ADP-ribose) polymerase-1 (PARP-1) activity

Overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) has been demonstrated to result in various stress-related diseases, including diabetes mellitus. Deficiency of cellular nicotinamide adenine dinucleotide (NAD(+)) content, consumed by PARP-1 to add ADP-ribose moieties onto target proteins, contributes to pathophysiological conditions. Adenosine thiamine triphosphate (AThTP) exists in small amounts in mammals; however, the function(s) of this metabolite remains unresolved. The structure of AThTP resembles NAD(+). Recent experimental studies demonstrate beneficial impacts of high-dose thiamine treatment of diabetic complications. These findings have led us to hypothesize that AThTP may modulate the activity of PARP-1. We have chemically synthesized AThTP and evaluated the effect of AThTP on recombinant PARP-1 enzyme activity. AThTP inhibited the PARP-1 activity at 10 μM, and a structural model of the PARP-1-AThTP complex highlighted the AThTP binding site. The results provide new insights into the pharmacological importance of AThTP as an inhibitor of PARP-1.     

Peripapillary crescent and related factors in highly myopic healthy eyes

Purpose

To investigate the relationship between the size of the peripapillary crescent and different ocular parameters in highly myopic healthy eyes; in addition, to determine whether the area of the peripapillary crescent enlarged significantly during one year of observation.

Methods

The medical records of 49 highly myopic healthy eyes whose fellow eyes had myopic complications were reviewed. The area of the peripapillary crescent and other ocular parameters were measured initially and after one year. The changes in the area of the peripapillary crescent and their association with other ocular parameters during the natural course of the pathological myopia were determined.

Results

The area of the peripapillary crescent was significantly associated with the choroidal thickness (P < 0.001), axial length (P < 0.001), and foveal thickness (P < 0.01). Stepwise regression analyses found that the factors most associated with the area of the peripapillary crescent were the choroidal thickness (P < 0.01) and the absolute nasal staphyloma height (P < 0.05). The factor most associated with the increase in the area of the peripapillary crescent was the increase in the axial length (P < 0.01).

Conclusions

The size of the peripapillary crescent may be affected by changes in the axial length, the height of the posterior staphyloma, and the choroidal thickness.