Early microchimerism in peripheral blood following kidney transplantation.

BACKGROUND: The role of microchimerism found in the peripheral blood of renal transplant recipients remains a matter of debate. We assessed the frequency of microchimerism after kidney transplantation and examined its influence on clinical courses over a 12-month follow-up period. PATIENTS AND METHODS: Ten single-kidney recipients underwent microchimerism detection at 2 days, 2 weeks, and 1, 3, 6, and 12 months after transplantation, with mismatch human leukocyte antigen (HLA)-A, -B, and -C used as markers. RESULTS: Microchimerism was detected in 8 (80%) patients at 2 days after kidney transplantation. In 3 of those, microchimerism became negative within 3 months after transplantation, whereas it remained present for up to 12 months in 3 patients (33 %). There was 1 acute rejection episode in a patient in whom microchimerism became negative within 3 months. Protocol renal graft biopsy specimens obtained 3 months after transplantation revealed no acute cellular-mediated rejection (ACMR) or acute antibody-mediated rejection (AAMR) in the 5 patients positive for microchimerism at 3 months. CONCLUSIONS: Microchimerism was frequently detected after kidney transplantation. Microchimerism that remained for more than 3 months post-transplantation might be correlated with a lower incidence of rejection, thus its monitoring may help identify recipients with a low rejection risk.

Evaluation of arterial stiffness after successful renal transplantation using brachial-ankle pulse wave velocity.

BACKGROUND: Cardiovascular disease remains a main cause of mortality in renal transplant recipients. Determination of aortic stiffness with pulse wave velocity (PWV) is considered a strong predictor of cardiovascular risk. We investigated arterial stiffness with brachial-ankle pulse wave velocity (baPWV) after successful renal transplantation. METHODS: We studied 197 patients (mean age = 53.2 ± 10.8 years) who underwent successful renal transplantation. baPWV was evaluated with a noninvasive automatic Omron Colin device. During follow-up (mean = 183.8 ± 108.9 months), we investigated parameters of sex, age, body mass index, duration before (dialysis) and after transplantation, and cardiovascular risk factors (hypertension and diabetes). In all subjects, fasting concentrations of serum creatinine, non-(HDL) high-density lipoprotein-cholesterol (total cholesterol minus HDL-cholesterol), low-density lipoprotein-cholesterol, and triglyceride were also compared with those at enrollment. RESULTS: Mean baPWV levels were 1519 ± 329 cm/s in our renal transplant recipients. baPWV increased independent of age, duration of dialysis before transplantation, and cardiovascular risk factors. Serum creatinine and dilation did not show any significant correlations to baPWV. CONCLUSION: In renal transplant recipients, baPWV may be more influenced by past clinical history before transplantation than by current condition. Noninvasive assessment of arterial stiffness with baPWV may be a useful and convenient indicator of cardiovascular disease after renal transplantation.

Low temperature affects the processing pattern and RNA editing status of the mitochondrial cox2 transcripts in wheat.

We investigated the effects of low temperature on the expression of mitochondria-encoded genes in wheat. During the course of our study, we found that the transcriptional pattern of cox2 was affected by low temperature. Northern blot analysis indicated that the precursor transcript before intron splicing was clearly increased by cold, although the level of mature message was not changed. We also found that cold treatment severely suppressed RNA editing at intron-binding site 1 of the precursor transcript, which plays an important role in intron splicing. These results suggest that low temperature could affect the post-transcriptional regulation of wheat mitochondrial cox2 transcripts, i.e. intron splicing and/or RNA editing.

Possible existence of a novel receptor for uridine analogues in the central nervous system using two isomers, N3-(S)-(+)- and N3-(R)-(-)-alpha-hydroxy-beta-phenethyluridines.

Uridine analogue binding sites, the so-called uridine receptor, were observed in the experiments on specific [3H]N3-phenacyluridine binding to bovine synaptic membranes using two isomers, N3-(S)-(+)- and N3-(R)-(-)-alpha-hydroxy-beta-phenethyluridine, as ligands. The potent hypnotic, N3-(S)-(+)-alpha-hydroxy-beta-phenethyluridine, but not the (R)-isomer, strongly inhibited [3H]N3-phenacyluridine binding. The racemate had inhibitory activity intermediate between that of the two alpha-hydroxy-beta-phenethyluridines ((R)- or (S)-isomers). The inhibitory constants of these compounds were determined. The Ki values of N3-phenacyluridine, alpha-hydroxy-beta-phenethyluridine (racemate), N3-(R)-(-)-, and N3-(S)-(+)-alpha-hydroxy-beta-phenethyluridine were 0.65, 397.4, 1908, and 10.2 nM, respectively. The present results indicate the existence of uridine receptors in the central nervous system in relation to their hypnotic activities reported previously.

Does circulating erythropoietin reflect progression of IgA nephropathy? Comparison with urinary N-acetyl-beta-D-glucosaminidase.

BACKGROUND: Recent reports describe that erythropoietin (Epo) is produced by peritubular interstitial fibroblast-like cells in response to a hypoxic stimulus. We studied serum Epo levels as a possible marker of tubulointerstitial damage in the progression of IgA nephropathy (IgAN), in comparison with urinary (u-) levels of N-acetyl-beta-D-glucosaminidase (NAG), which is mainly derived from proximal tubular cells and is used as a marker of tubular damage. METHODS: Thirty-eight patients with IgA nephropathy (IgAN) with relatively preserved renal function (serum creatinine: sCr, 0.5-2.2 mg/dl) were examined. The severity of glomerulosclerosis and interstitial fibrosis of the renal biopsy tissue was expressed by semiquantitative grading scores. Clinical parameters including serum creatinine (sCr), blood pressures, and 24-h proteinuria levels were obtained at the renal biopsy. Epo was measured by a radioimmunoassay (RIA) of sera obtained in the morning and u-NAG was measured by colorimetric method of 24-h urine samples. RESULTS: The mean Epo level of the patients (17.7+/-6.3 mU/ml) was not different from the control level (19.3+/-3.7 mU/ml). There were no significant correlations between Epo levels and red blood cell (RBC) counts, haematocrit (Hct), or haemoglobin (Hb) levels. The mean u-NAG level of the patients (6.7+/-6.2 U/gCr) was significantly higher than the control level (1.9+/-0.5 U/gCr). There was an inverse quantitative correlation between Epo and u-NAG levels in the patients (P<0.02). The u-NAG levels showed quantitative positive correlations with sCr (P<0.001), u-proteins (P<0.001), systolic (SBP) (P<0.001), and diastolic blood pressures (DBP) (P<0.05). Conversely, Epo levels were inversely correlated with sCr, SBP and DBP (each P<0.05). The patients with higher u-proteins (>2.0 g/day) showed significantly decreased Epo levels (P<0.05) than those with lower u-proteins (<2.0 g/day). The both scores of glomerulosclerosis and interstitial fibrosis were positively correlated with the u-NAG levels (each P<0.001), but were not correlated with the Epo levels. CONCLUSIONS: The significant correlation between u-NAG and serum Epo levels suggests that tubular damage and interstitial cell dysfunction are associated each other in the progression of IgAN. Serum Epo levels bearing inverse correlations with sCr, blood pressure levels and heavy proteinuria seem to reflect clinical severity of IgAN, whereas u-NAG can be more useful progression marker of IgAN bearing correlations with both clinical and histological findings.

AIDS policy in Japan: integration within structured paternalism.

Structured paternalism consists of the setting of public policy by centralized authority without the benefit of surveillance and research to guide it. It is a concept deeply embedded in Japanese society, based on the belief that the central government is the highest authority. It strongly affects decision-making regarding medical care, in that many policies are set without the guidance of either the public at large or physicians and scientists. The 1990s, however, have seen a diminution of this structured paternalism, as is illustrated by public policy regarding AIDS. The general public is becoming more knowledgeable about this disease and has become more willing to voice its opinion and even take action. The government, in particular the Ministry of Health and Welfare, is becoming more responsive to public and expert opinion. Individual providers within the medical profession are often succeeding in providing excellent medical care to HIV/AIDS patients despite a lack of well-conceived guidelines.