Size and stabilization of the dorsoulnar fragment in AO C3-type distal radius fractures.

INTRODUCTION: Volar locking plate (VLP) fixation has become the gold-standard treatment for distal radius fractures (DRFs). Especially, internal fixation of the volar lunate facet fragment is essential for the treatment of AO C3-type DRFs. On the other hand, the necessity of the fixation of the dorsal lunate facet fragment (dorsoulnar fragment) remains unclear. The purpose of the present study was to measure three-dimensionally the size of the dorsoulnar fragments in AO C3-type DRFs using computed tomography (CT) images in detail, and to reveal relationships of the size and stabilization of the dorsoulnar fragment with postoperative fracture displacement after VLP fixation. MATERIALS AND METHODS: We retrospectively reviewed the 101 consecutive Japanese patients who underwent surgical treatment for AO C3-type distal radius fractures. If patient had dorsoulnar fragment, the three-dimensional size of this fragment and the occupying ratio to the radiocarpal joint (RCJ) and the distal radioulnar joint (DRUJ) were anatomically evaluated using the preoperative CT images. In addition, we investigated the relationship of the size and stabilization of the dorsoulnar fragment with fracture displacement after VLP fixation. We statistically compared the size parameters and occupying ratio of the dorsoulnar fragment between the displaced group and the stable groups using a two-tailed t-test. We also statistically compared the numbers of screws inserted into the dorsoulnar fragments between the displaced and stable groups using a chi-square test. RESULTS: The mean dorsoulnar fragment size was 9.4 mm × 7.9 mm × 11.0 mm and the occupying ratio to the DRUJ and RCJ was 50% and 10%, respectively. The number of patients treated with volar locking plate fixation was 77, of which 12 patients had postoperative displacements. Although the size of the dorsoulnar fragment was not associated with postoperative displacement, stabilization following screw insertion into the dorsoulnar fragment was significantly associated with displacement. CONCLUSION: Stabilization of the dorsoulnar fragment with at least one screw of the volar locking plate was necessary to prevent postoperative fracture displacement regardless of dorsoulnar fragment size in AO C3-type distal radius fractures.

Gongylonema infection of wild mammals in Japan and Sardinia (Italy).

The gullet worms, classical Gongylonema pulchrum and newly differentiated Gongylonema nepalensis, are prevalent in various mammals in Japan and Sardinia, Italy, respectively. The former species is cosmopolitan in distribution, dwelling in the mucosa of the upper digestive tract of a variety of domestic and wild mammals, and also humans. At present, the geographical distribution of G. nepalensis is known in Nepal and Sardinia, with the nematode having been recorded from the oesophagus of water buffaloes (Nepal), cattle, sheep, goats and wild mouflon (Sardinia). To clarify their natural transmission cycles among domestic and wild mammals, the present study analysed the ribosomal RNA gene (rDNA) and mitochondrial cytochrome c oxidase subunit 1 gene (cox1) of worms of various origins: G. pulchrum worms from sika deer, wild boars, Japanese macaques, and feral alien Reeves's muntjacs in Japan, and G. nepalensis worms from a red fox and a wild boar in Sardinia. Although the internal transcribed spacer (ITS) regions of rDNA and partial cox1 nucleotide sequences of G. pulchrum from native wild mammals in Japan were distinct from those of the worms in cattle, the worms from feral alien Reeves's muntjacs showed the cattle-type ITS genotype and cox1 cattle-I and II haplotypes. The rDNA and cox1 nucleotide sequences of G. nepalensis from a red fox in Sardinia were almost identical to those of the worms from domestic and wild ruminants on the island. The ecological interaction between domestic and wild mammals and their susceptibility to different Gongylonema spp. must be considered when trying to elucidate this spirurid's transmission dynamics in nature.

Molecular genetic conspecificity of Spiculopteragia houdemeri (Schwartz, 1926) and S. andreevae (Drózdz, 1965) (Nematoda: Ostertagiinae) from wild ruminants in Japan.

Male dimorphism of the subfamily Ostertagiinae (Nematoda: Trichostrongylidae) is a well-known phenomenon, and two or more morphotypes of a single species have previously been described as different species. Two Spiculopteragia spp., S. houdemeri (syn. S. yamashitai) and S. andreevae (syn. Rinadia andreevae) recorded in Asian cervids and wild bovids, are considered to represent major and minor morphs of S. houdemeri, respectively, based solely on their co-occurrence in the same host individual along with monomorphic females. In this study, males of morph houdemeri ( = S. houdemeri) and morph andreevae ( = S. andreevae) as well as females with three different vulval ornamentations were collected from sika deer (Cervus nippon) and Japanese serows (Capricornis crispus) distributed on the mainland of Japan. Morphologically characterized worms were subjected to molecular genetic analyses based on the internal transcribed spacer region of the ribosomal RNA gene and a partial region of the cytochrome c oxidase subunit I gene of mitochondrial DNA. Of 181 collected sika deer, 177 (97.8%) and 73 (40.3%) deer harboured males of morphs houdemeri and andreevae, respectively. Worm numbers of the former morph were found to range between 1 and 444 per individual, whereas only 1-25 worms per individual were detected for the latter morph. Five out of six serows harboured 47-71 or 2-9 males of morphs houdemeri and andreevae per individual, respectively. Females with one or two vulval flaps were predominant, but there was a substantial presence of flapless females in both host species. All the morphs of male and female adults had an identical genetic background, thus directly confirming the morphological polymorphism of S. houdemeri.

Genetic variation of Gongylonema pulchrum from wild animals and cattle in Japan based on ribosomal RNA and mitochondrial cytochrome c oxidase subunit I genes.

The gullet worm (Gongylonema pulchrum) has been recorded from a variety of mammals worldwide, including monkeys and humans. Due to its wide host range, it has been suggested that the worm may be transmitted locally to any mammalian host by chance. To investigate this notion, the ribosomal RNA gene (rDNA), mainly regions of the internal transcribed spacers (ITS) 1 and 2, and a cytochrome c oxidase subunit I (COI) region of mitochondrial DNA of G. pulchrum were characterized using parasites from the following hosts located in Japan: cattle, sika deer, wild boars, Japanese macaques, a feral Reeves's muntjac and captive squirrel monkeys. The rDNA nucleotide sequences of G. pulchrum were generally well conserved regardless of their host origin. However, a few insertions/deletions of nucleotides along with a few base substitutions in the ITS1 and ITS2 regions were observed in G. pulchrum from sika deer, wild boars and Japanese macaques, and those differed from G. pulchrum in cattle, the feral Reeves's muntjac and captive squirrel monkeys. The COI sequences of G. pulchrum were further divided into multiple haplotypes and two groups of haplotypes, i.e. those from a majority of sika deer, wild boars and Japanese macaques and those from cattle and zoo animals, were clearly differentiated. Our findings indicate that domestic and sylvatic transmission cycles of the gullet worm are currently present, at least in Japan.

Effects of amlodipine and valsartan on vascular damage and ambulatory blood pressure in untreated hypertensive patients.

The present study was performed to compare the long-term effects of 24-h ambulatory blood pressure (BP) control with amlodipine versus valsartan on vascular damage in untreated hypertensive patients. Amlodipine and valsartan have benefits on cardiovascular mortality and morbidity in hypertensive patients. Although ambulatory BP is associated with severity of target-organ damage in hypertensive patients, beneficial effects of ambulatory BP control with amlodipine versus valsartan on vascular damage have not been compared. Pulse wave velocity (PWV), intima-media thickness (IMT) of the carotid arteries, urinary albumin excretion (UAE) and 24-h ambulatory BP were determined in 100 untreated hypertensive patients before and 12 months after the start of antihypertensive therapy with amlodipine or valsartan. Amlodipine and valsartan decreased ambulatory BP similarly, but the variability of 24-h and daytime ambulatory systolic BP was significantly reduced by amlodipine but not by valsartan. The reduced variability of ambulatory systolic BP caused by amlodipine significantly contributed to the improvement of PWV, although both drugs decreased PWV similarly. Carotid IMT was unaffected by treatment with either drug. Valsartan significantly decreased UAE independently of its depressor effect, but amlodipine had no effect on UAE. These results suggest that the 24-h control of ambulatory BP with amlodipine had functionally improved the stiffened arteries of hypertensive patients by the end of 12 months of treatment, in part through reducing BP variability, whereas ambulatory BP control with valsartan decreased the arterial stiffness to the same degree as amlodipine without affecting BP variability maybe through some pleiotropic effects.

Increased expression of cyclooxygenase-2 in the renal cortex of human prorenin receptor gene-transgenic rats.

Increased macula densa cyclooxygenase-2 (COX-2) is observed in diabetic rats and may contribute to hyperfiltration states. However, the signals mediating increased COX-2 expression in diabetic rats remain undetermined. We recently found that non-proteolytic activation of prorenin by site-specific binding proteins, such as prorenin receptor, plays a pivotal role in the development of diabetic nephropathy. The present study was designed to determine the contribution of prorenin receptor to renal cortical COX-2 expression. The COX-2 mRNA and protein levels of six 4-week-old male wild-type rats and six human prorenin receptor gene-transgenic (hProRenRcTg) rats were measured by real-time polymerase chain reaction methods, Western blotting, and immunohistochemistry, and compared. There were no differences between the two groups in arterial pressure measured by telemetry, urinary sodium excretion, or renal levels of rat prorenin receptor mRNA. The renal cortical COX-2 mRNA levels of the hProRenRcTg rats were significantly higher than those of the wild-type rats, and the renal cortical COX-2 protein levels were also higher in hProRenRcTg rats than in the wild-type rats. Immunohistochemical analysis revealed that COX-2 immunostaining was predominantly present in the macula densa cells, and significantly more COX-2-positive cells were present in the hProRenRcTg rats than in the wild-type rats. In addition, COX-2 inhibition with NS398 significantly decreased renal cortical blood flow in the hProRenRcTg rats but not in the wild-type rats. These results strongly suggest that human prorenin receptor directly or indirectly contributes to the regulation of renal cortical COX-2 expression.

Ambulatory blood pressure variability and brachial-ankle pulse wave velocity in untreated hypertensive patients.

Blood pressure (BP) variability is estimated as the standard deviation of 24-h ambulatory BP. The present study was performed to determine the effect of the mean 24-h ambulatory BP values and standard deviations on arterial wall stiffness assessed by brachial-ankle pulse wave velocity (baPWV). Brachial-ankle pulse wave velocity, carotid intima-media thickness (IMT), urinary albumin excretion (UAE) and 24-h ambulatory BP were measured before the start of antihypertensive therapy in 203 newly diagnosed hypertensive patients (53.3+/-0.7 years old; clinic systolic/diastolic BP: 154+/-1/98+/-1 mm Hg), and univariate and multivariate regression analyses of these clinical and biological parameters were performed. Univariate regression analyses revealed a significant association between mean baPWV values and the standard deviations of ambulatory systolic/diastolic BP. Mean ambulatory systolic/diastolic BP values were also associated with UAE, and the standard deviations of ambulatory systolic BP were associated with maximum carotid IMT. Quintile analyses showed that patients with a mean 24-h ambulatory mean BP value and standard deviation below 110 and 20 mm Hg, respectively, had the lowest baPWV. Moreover, the multivariate regression analyses confirmed a significant correlation between baPWV and the standard deviation of 24-h ambulatory systolic BP. In conclusion, untreated hypertensive patients with a higher 24-h ambulatory systolic BP variability had stiffer arterial walls. Ambulatory systolic BP variability may be involved in stiffening of the arteries of hypertensive patients.

Long-term effects of statins on arterial pressure and stiffness of hypertensives.

Although lowering blood pressure (BP) reduces aortic stiffness, achieving the recommended BP goal can be difficult. Recent studies have shown that short-term use of statins can reduce BP significantly. To determine the long-term effects of statins on BP and aortic stiffness, a single-blind randomized prospective study was performed on 85 hyperlipidaemic hypertensive patients whose BP was insufficiently controlled by antihypertensive therapy. Every 3 months, aortic stiffness was assessed by measuring pulse wave velocity (PWV). Patients were randomly allocated to groups treated with pravastatin, simvastatin, fluvastatin, or a nonstatin antihyperlipidaemic drug. No significant differences in patient characteristics, kinds of antihypertensive drugs, BP, ankle brachial index, PWV, or serum lipid, creatinine, or C-reactive protein levels were found between the four groups at the start of the study. During the 12-month treatment period, PWV did not change in the pravastatin group or nonstatin group, but it was transiently reduced in the simvastatin group and significantly decreased in the fluvastatin group, even though the doses of the statins used in this study were lower than the usually prescribed dose. All four antihyperlipidaemic drugs significantly decreased serum cholesterol levels without affecting BP, ankle brachial index, or serum triglyceride levels. The C-reactive protein serum levels decreased significantly in the three statin groups but not in the nonstatin group. These results suggest that long-term use of fluvastatin by hyperlipidaemic hypertensive patients is associated with a significant reduction in aortic stiffness without any effect on BP.

Domain reactivity of autoantibodies to calpastatin in patients with systemic rheumatic diseases.

Abstract Autoantibodies to calpastatin (endogenous inhibitor of calpain, a calcium-dependent neutral proteinase) have been detected in sera of patients with rheumatoid arthritis (RA) and other diseases. We investigated the epitope reactivity of anticalpastatin autoantibodies in patients with rheumatic diseases. cDNAs encoding each calpastatin domain (L, I, II, III, and IV) were amplified by PCR and ligated into an expression vector. The fusion proteins were expressed in E. coli. The presence of autoantibodies specific for each calpastatin domain was assayed in sera of patients with various rheumatic diseases by immunoblotting the fusion proteins with these sera. Of the RA patient sera, 81% reacted with at least one calpastatin domain. This reaction was significantly greater than with sera from patients with systemic lupus erythematosus (46%), scleroderma (32%), polymyositis/dermatomyositis (43%), and normal controls (13%). Domains I and II were recognized by RA patient sera significantly more than by other patient sera, whereas domains III and IV reacted almost equally among all patient sera. Although, collectively, sera from RA and lupus patients reacted equally with all domains, scleroderma sera tended to react with only domains I and IV and myositis sera tended to recognize only domains III and IV. Patients with RA positive for anticalpastatin antibodies exhibited more active disease (i.e., a higher erythrocyte sedimentation rate and C-reative protein level) than antibody-negative patients. Our results suggest that anticalpastatin antibodies were detected in RA with the highest frequency and that different domain reactivity was shown among different diseases. The presence of these antibodies in sera may be related to the type of disease and, in RA, with disease activity, suggesting their importance in rheumatic disorders.

Total parenteral nutrition supplemented with medium-chain triacylglycerols prevents atrophy of the intestinal mucosa in septic rats.

Total parenteral nutrition (TPN) is associated with an increased incidence of bacterial translocation (BT) compared with enteral nutrition because of the disuse atrophy of the intestine. In this study, we assessed the effect of adding medium-chain triacylglycerols (MCT) to TPN for the prevention of mucosal atrophy in the intestine. Rats were subjected to either fat-free TPN, TPN with long-chain triacylglycerols (LCT), or TPN with MCT for 5 d and nutrition parameters were evaluated. In another set of rats receiving the same TPN regimen, 0.8 or 0.05 mg/kg endotoxin was administered on day 4. Survival was evaluated and BT to the mesenteric lymph nodes, liver, and systemic blood was measured 24 h later. The mucosal heights of the jejunum and ileum were evaluated concurrently. The survival rate was significantly improved in the MCT group (P < 0.05) at the endotoxin dose of 0.8 mg/kg. The nutrition condition presented by phospholipid, total cholesterol, and total ketone body levels was the best in the MCT group compared to the other groups. The intestinal villous height in the ileum was significantly greater in the MCT group. However, the improvement of BT in MCT group was not statistically significant. In this endotoxin-challenged rat model, survival rate was improved by the supplementation of MCT. This effect may be presented in some part by the improvement in nutrition condition and by the prevention of mucosal atrophy in the intestine.

Augmentation of mitochondrial reduced glutathione by S-adenosyl-L-methionine administration in ischemia-reperfusion injury of the rat steatotic liver induced by choline-methionine-deficient diet.

We examined whether warm ischemia-reperfusion (I/R) damage of the rat steatotic liver can be reduced by administration of S-adenosyl-L-methionine (SAMe). We examined the effect of SAMe on the mitochondrial reduced-glutathione (GSH) pool. Sixty minutes of partial left lobar vascular clamping followed by 2 h of reperfusion were employed for a model of hepatic warm ischemia. Either 5% dextrose or SAMe was injected intraperitoneally 2 h before I/R in steatotic rats (S-D5% or S-SAMe group). Serum liver enzyme concentrations 2 h after reperfusion were significantly lower in the S-SAMe group than in the S-D5% group. The cytosolic and mitochondrial GSH concentrations after I/R were significantly higher in the S-SAMe group than in the S-D5% group (p < 0.05). The cytosolic and mitochondrial oxidized-glutathione/GSH ratios after I/R were significantly greater in the S-D5% group than in the S-SAMe group (p < 0.01). The adenosine triphosphate concentration was higher in the S-SAMe group than in the S-D5% group (p = 0.0515). These results show that hepatocellular and mitochondrial oxidative stress after I/R in the steatotic liver can be reduced by administration of SAMe. The results also show that mitochondrial function and hepatocellular integrity can be restored by administration of SAMe in steatotic rats.