Regional arterial stiffness in patients with type 2 diabetes and chronic kidney disease

Increased arterial stiffness is an independent predictor of death from cardiovascular disease, and aortic stiffness is more predictive than stiffness of other arterial regions. Because little is known about the effect of chronic kidney disease (CKD) on regional arterial stiffness, pulse wave velocity (PWV) of four different arterial segments was measured in patients who had type 2 diabetes with and without various stages of CKD. A total of 434 patients had type 2 diabetes, and there were 192 healthy control subjects who were comparable in age and gender. GFR was estimated by the abbreviated Modification of Diet in Renal Disease equation. The patients with diabetes were classified into CKD stages by the definition of the Kidney Disease Outcomes Quality Initiative guidelines. PWV was measured in the heart-femoral, heart-carotid, heart-brachial, and femoral-ankle segments simultaneously using an automatic pulse wave analyzer. PWV of each arterial region was increased in patients who had diabetes without kidney damage and was increased further in a stepwise manner with the advanced stages of CKD. The increase in PWV was greater in the heart-femoral and heart-carotid regions than in the heart-brachial and femoral-ankle segments. However, after adjustment for age, BP, and other confounding factors using a multiple regression model, decreased GFR was independently associated with increased PWV of the heart-femoral region but not with PWV of other arterial segments. In type 2 diabetes, CKD was associated with increased stiffness of arteries, particularly of the aorta. The cross-sectional result may explain the increased risk for cardiovascular disease in CKD, although longitudinal studies are needed to confirm it.     

Reconstruction of a natural-appearing umbilicus using an island flap: case report.

A case of successful reconstruction of the umbilicus using a depressed scar in an 11-year-old girl with a large and rigid scar spreading around the centre of the abdominal wall is presented. The anatomical umbilicus was replaced by a large scar after a previous surgery for umbilical cord hernia. The difficulty of the conventional method compelled us to use a distant scar dimple as an island flap. In addition, the three-dimensional morphology of the umbilicus could be reproduced by rolling a spindle island flap into a cone. Postoperatively, the reconstructed umbilicus has remained deep and aesthetically well shaped.     

Comparison of ramosetron and azasetron for prevention of acute and delayed cisplatin-induced emesis in lung cancer patients

We performed a retrospective study that compared the efficacy and safety of ramosetron with azasetron in a case of acute and delayed emesis induced by cisplatin (CDDP)-included chemotherapy in patients with lung cancer. The study subjects were 100 lung cancer patients treated with combination therapy of cisplatin, ifosfamide, irinotecan (CIC therapy). The ramosetron group and azasetron group received, respectively, ramosetron 0.3 mg or azasetron 10 mg intravenous injection, 30 minutes prior to CDDP. All patients received 32 mg of dexamethasone intravenously. Protection from emesis showed no significant difference between two treatment groups. However, the grade of nausea was significantly lower in the ramosetron group than in the azasetron group. Furthermore, chlorpromazine hydrochloride for use as a rescue medication was required by significantly fewer in the ramosetron group than in the azasetron group. Adverse effects were observed in 27 cases in the ramosetron group and 24 cases in the azasetron group. However, because the symptoms were all mild, we did not consider there was any safety problem. In conclusion, it was suggested that ramosetron is a clinically useful treatment for acute and delayed emesis induced by cisplatin-induced chemotherapy in patients with lung cancer.     

Comparative investigation of inhibitors of extracerebral dopa decarboxylase in man and rats

The decarboxylase inhibitor Ro 4–4602 [N¹-(dl -seryl)-N²-(2,3,4-trihydroxybenzyl)hydrazine] in doses of 3.4–34.0 μmol/kg (1–10mg/kg) progressively enhances the increase of dopa and 3-O-methyldopa and diminishes the rise of phenolcarboxylic acids in human plasma induced by administration of l -dopa. A dose of 3.4 μmol/kg Ro 4–4602 is approximately equipotent to 17.0 μmol/kg MK 485 [β-(3,4-dihydroxyphenyl)-α-hydrazino-α-methyl-dl -propionie acid]. Ro 4–4602, combined with 2 mg/kg l -dopa, causes a higher increase of catecholamines than 20 mg/kg l -dopa alone in the striatum and probably in the hypothalamus of rat brain, whereas in the other brain areas the amine rise is equal after both treatments. MK 485 in doses equimolar to Ro 4–4602 has a less marked effect in all brain areas. Either inhibitor (10–2 μmol/kg) combined with 2 mg/kg l -dopa causes markedly less increase of catecholamines than 20 mg/kg l -dopa alone in the rat heart. Ro 4–4602, in small single doses, used at present in the treatment of Parkinson's syndrome, markedly inhibits the extracerebral decarboxylation of l -dopa in man and rats and is more potent than MK 485.     

Role of rBAT Gene Products in Cystinuria

To investigate whether rBAT gene products function as a crystine transporter component or as a transport activator, we microinjected several C–terminal deletion mutants of rBAT cRNA into Xenopus oocytes, and measured transport activity for arginine, leucine and cystine in the presence and absence of sodium. Wild type rBAT significantly stimulated the uptake of all 3 amino acids 10–20 fold compared to control mutants. On the other hand, no mutant, except a Δ511–685 mutant, stimulated the uptake of these amino acids. However, the Δ511–685 mutant significantly increased the uptake of arginine. In the presence of sodium, the Δ511–685 mutant also increased the uptake of leucine. The Δ511–685 mutant did not stimulate crystine uptake in the presence and absence of sodium. Furthermore, inhibition of L–arginine uptake by L–homoserine was seen only in the presence of sodium. These results suggest that mutant rBAT stimulates the endogenous amino acid transport system y⁺ in oocytes. Finally, rBAT gene products, as the primary cause of cystinuria, may function as activators of the amino acid transport system in renal brush border membrane.