Influence of surgical orthodontic treatment on masticatory function in skeletal Class III patients.

Skeletal Class III patients exhibit malocclusion characterised by Angle Class III and anterior crossbite, and their occlusion shows total or partially lateral crossbite of the posterior teeth. Most patients exhibit lower bite force and muscle activity than non-affected subjects. While orthognathic surgery may help improve masticatory function in these patients, its effects have not been fully elucidated. The aims of the study were to evaluate jaw movement and the electromyographic (EMG) activity of masticatory muscles before and after orthognathic treatment in skeletal Class III patients in comparison with control subjects with normal occlusion. Jaw movement variables and EMG data were recorded in 14 female patients with skeletal Class III malocclusion and 15 female controls with good occlusion. Significant changes in jaw movement, from a chopping to a grinding pattern, were observed after orthognathic treatment (closing angle P < 0.01; cycle width P < 0.01), rendering jaw movement in the patient group similar to that of the control group. However, the grinding pattern in the patient group was not as broad as that of controls. The activity indexes, indicating the relative contributions of the masseter and temporalis muscles (where a negative value corresponds to relatively more temporalis activity and vice versa) changed from negative to positive after treatment (P < 0.05), becoming similar to those of control subjects. Our findings suggest that orthognathic treatment in skeletal Class III patients improves the masticatory chewing pattern and muscle activity. However, the chewing pattern remains incomplete compared with controls.

First molar cross-bite is more closely associated with a reverse chewing cycle than anterior or pre-molar cross-bite during mastication.

A posterior cross-bite is defined as an abnormal bucco-lingual relationship between opposing molars, pre-molars or both in centric occlusion. Although it has been reported that patients with unilateral posterior cross-bite often show unique chewing patterns, the relationship between the form of cross-bite and masticatory jaw movement remains unclear in adult patients. The objective of this study was to investigate masticatory jaw movement among different forms of cross-bite. One hundred and one adults were recruited in this study: 27 had unilateral first molar cross-bite (MC group); 28, unilateral pre-molar cross-bite (PC group); 23, anterior cross-bite (AC group); and 23, normal occlusion (control group). Masticatory jaw movement of the lower incisor point was recorded with six degrees of freedom jaw-tracking system during unilateral mastication. Our results showed that the reverse chewing ratio during deliberate unilateral mastication was significantly larger in the MC group than in the PA (P < 0.001), AC (P < 0.001) and control (P < 0.001) groups. These findings suggest that compared to the anterior or pre-molar cross-bite, the first molar cross-bite is more closely associated with a higher prevalence of a reverse chewing cycle.

Influence of maximum bite force on jaw movement during gummy jelly mastication.

It is known that maximum bite force has various influences on chewing function; however, there have not been studies in which the relationships between maximum bite force and masticatory jaw movement have been clarified. The aim of this study was to investigate the effect of maximum bite force on masticatory jaw movement in subjects with normal occlusion. Thirty young adults (22 men and 8 women; mean age, 22.6 years) with good occlusion were divided into two groups based on whether they had a relatively high or low maximum bite force according to the median. The maximum bite force was determined according to the Dental Prescale System using pressure-sensitive sheets. Jaw movement during mastication of hard gummy jelly (each 5.5 g) on the preferred chewing side was recorded using a six degrees of freedom jaw movement recording system. The motion of the lower incisal point of the mandible was computed, and the mean values of 10 cycles (cycles 2-11) were calculated. A masticatory performance test was conducted using gummy jelly. Subjects with a lower maximum bite force showed increased maximum lateral amplitude, closing distance, width and closing angle; wider masticatory jaw movement; and significantly lower masticatory performance. However, no differences in the maximum vertical or maximum anteroposterior amplitudes were observed between the groups. Although other factors, such as individual morphology, may influence masticatory jaw movement, our results suggest that subjects with a lower maximum bite force show increased lateral jaw motion during mastication.

Posterior scissors-bite: masticatory jaw movement and muscle activity.

Scissors-bite is a malocclusion characterised by buccal inclination or buccoversion of the maxillary posterior tooth and/or linguoclination or linguoversion of the mandibular posterior tooth. This type of malocclusion causes reduced contact of the occlusal surfaces and can cause excessive vertical overlapping of the posterior teeth. This case-control study is the first to evaluate both masticatory jaw movement and masseter and temporalis muscle activity in patients with unilateral posterior scissors-bite. Jaw movement variables and surface electromyography data were recorded in 30 adult patients with unilateral posterior scissors-bite malocclusion and 18 subjects with normal occlusion in a case-control study. The chewing pattern on the scissors-bite side significantly differed from that of the non-scissors-bite side in the patients and of the right side in the normal subjects. These differences included a narrower chewing pattern (closing angle, P < 0.01; cycle width, P < 0.01), a longer closing duration (P < 0.05), a slower closing velocity (P < 0.01) and lower activities of both the temporalis (P < 0.05) and the masseter (P < 0.05) muscles on the working side. In 96% of the patients with unilateral posterior scissors-bite, the preferred chewing side was the non-scissors-bite side (P = 0.005). These findings suggest that scissors-bite malocclusion is associated with the masticatory chewing pattern and muscle activity, involving the choice of the preferred chewing side in patients with unilateral posterior scissors-bite.

Na(+)-H+ antiport activity in skin fibroblasts from blacks and whites.

The predisposition of black people to salt (NaCl)-sensitive essential hypertension may relate to racial differences in cellular Na+ metabolism. This tenet was investigated by examining the Na(+)-H+ antiport in serially passed skin fibroblasts from blacks and whites. Na(+)-dependent stimulation of the Na(+)-H+ antiport by cellular acidification resulted in a greater maximal velocity (Vmax) (mean +/- SEM) of this transport system in quiescent fibroblasts from blacks than fibroblasts from whites; the Vmax for recovery from cellular pH (pHi) of 6.6 was 5.84 +/- 0.50 versus 4.39 +/- 0.34 mmol H+/l X 20 seconds for blacks and whites, respectively (p less than 0.05). Although the Na+ concentration producing 50% stimulation of the Na(+)-H+ antiport for blacks (35.1 +/- 5.7 mM) was greater than for whites (24.1 +/- 3.5 mM), this difference was not statistically significant. No racial differences were observed in the Hill coefficient (n, 1.35 +/- 0.21 for blacks and 1.46 +/- 0.28 for whites). Compared with whites, cells from blacks exhibited a greater response to cytoplasmic acidification over the range of pHi values 6.20-6.60, as exhibited by an augmented rate of recovery in the pHi. These differences were not due to different basal pHi values or cellular buffering capacities, which were similar for blacks and whites. Na(+)-H+ antiport activity was not correlated with family history of hypertension. Increased activity of the Na(+)-H+ antiport in fibroblasts from blacks was confirmed without cellular acidification by stimulating quiescent cells with 10% human serum. This study demonstrates innate racial differences in cellular membrane Na(+)-H+ antiport activity.

Variations in the apparent pH set point for activation of platelet Na-H antiport.

To explore the role of the Na-H antiport in essential hypertension, we studied the kinetics of cytosolic pH and external sodium activation of this transport system in platelets from 65 normotensive and essential hypertensive subjects on and off antihypertensive medications. Subjects included both blacks and whites, as well as men and women. The fluorescent dye 2'7-bis(carboxyethyl)-5,6-carboxyfluorescein was used to monitor the cytosolic pH in these cells. Platelets from black (hypertensive and normotensive) men and hypertensive white men demonstrated a highly significant alkaline shift in the apparent cytosolic pH set point for activation of the Na-H antiport. For the hypertensive subgroups, the cytosolic pH set point values (mean +/- SEM) were: white men, 7.45 +/- 0.052; white women, 7.04 +/- 0.089; black men, 7.66 +/- 0.148; and black women, 7.20 +/- 0.082. For the normotensive subgroups, the cytosolic pH set point values were: white men, 7.13 +/- 0.034; white women, 7.05 +/- 0.036; black men, 7.50 +/- 0.110; and black women, 7.20 +/- 0.176 (p = 0.0016 for race and p = 0.0001 for gender, using a three-way analysis of variance by race, gender, and hypertension). There were no race-, gender-, or blood pressure-related differences among the various cohorts in the kinetics of sodium activation of the Na-H antiport, the cellular buffering power, and basal pH. These results suggest that at basal pH the Na-H antiport is quiescent in platelets from both black and white women and normotensive white men.(ABSTRACT TRUNCATED AT 250 WORDS)

Lower Na(+)-H+ antiport activity in vascular smooth muscle cells of Wistar-Kyoto rats than spontaneously hypertensive and Wistar rats.

To determine whether increased Na(+)-H+ antiport activity in vascular smooth muscle cells may relate to the pathogenesis of hypertension in the spontaneously hypertensive rat (SHR), we monitored Na(+)-dependent alkalinization of acidified cells from the hypertensive strain and two normotensive controls, the Wistar-Kyoto rat (WKY) and the Wistar rat. Changes in intracellular pH (pHi) of cultured aortic cells were measured using the fluorescent probe 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The initial maximal reaction velocity of Na(+)-dependent alkalinization was significantly higher in SHR and Wistar than WKY cells. Similar results were obtained for the maximal velocity of the proton equivalent efflux: SHR, 7.51 +/- 0.71; Wistar, 9.14 +/- 0.85; WKY, 4.38 +/- 0.55 mmol H+/liter x 10 s. There were no differences in the basal pHi or cellular buffering power among the three rat strains. These findings indicate that the activity of the Na(+)-H+ antiport is higher in SHR vascular smooth muscle cells than in WKY cells. However, by itself, this difference cannot explain the hypertensive process in the SHR, since this transport system is also higher in vascular cells of the Wistar rat.

Granulocyte colony-stimulating factor-producing primary pericardial mesothelioma.

A 54-year-old male patient presented with a granulocyte colony-stimulating factor (G-CSF)-producing primary pericardial mesothelioma, while showing symptoms of congestive heart failure, a fever of 38 to 39 degrees C, and marked leucocytosis of 52.7 x 10(3) cells/mm3. The histopathologic diagnosis was established after autopsy. G-CSF production was confirmed by the expression of G-CSF mRNA in the tumor extract and the patient's high serum G-CSF concentration. The expression of G-CSF by benign and malignant mesothelial cells has already been reported. However, this is the first case report of G-CSF production in a pericardial mesothelioma.

Evidence for amelioration of endothelial cell dysfunction by erythropoietin therapy in predialysis patients.

Evidence for the involvement of endothelial cells in the pathogenesis or erythropoietin-induced hypertension, and for endothelial cell damage in patients with chronic renal failure, has emerged and appears to be of major concern. We, therefore, investigated the effect of recombinant human erythropoietin (rHuEPO) therapy on endothelium-derived hormones in predialysis patients with progressive renal anemia. At the entry to the trial, the serum thrombomodulin concentration (Tm) and plasma endothelin-1 concentration (ET-1) in the predialysis patients were significantly higher than those in age- and sex-matched normal subjects. Following a 16 week period of treatment with 6000IU rHuEPO given intravenously once a week, patients' hematocrit increased from 27.1 +/- 2.6% to 34.6 +/- 3.2% (n = 16, P < .001). A positive correlation was found between Tm and serum creatinine concentration (Cr) (r = 0.61, P < .05 (n = 16), but no correlation was found between ET-1 and Cr. Tm and Tm/Cr significantly decreased from 7.9 +/- 2.8 ng/mL to 6.6 +/- 2.4 ng/mL (P < .01, n = 16), and from 2.1 +/- 0.7 (x10(-10) to 1.6 +/- 0.7 (x10(-10), P < .01, n = 16), respectively. However, there was no change in ET-1 as a result of the rHuEPO therapy. Creatinine clearance (Ccr), Cr, total amount of daily Tm excretion, Tm clearance/Ccr, daily urinary protein and albumin excretion, and blood pressure also remained unchanged throughout the trail. The present study indicates that correcting anemia by rHuEPO therapy reduces an abnormally elevated Tm in predialysis patients while blood pressure and renal function remain unchanged, suggesting that rHuEPO has a beneficial effect on endothelial cell dysfunction in chronic renal failure patients. This effect may be mediated via an improved oxygen supply to the endothelial cells due to the amelioration of anemia by rHuEPO.

Association of angiotensinogen gene polymorphism with erythropoietin-induced hypertension: a preliminary report.

The association of the angiotensinogen (AGT) gene variation at codon 235, the T235 variant, with hypertension induced by erythropoietin (Epo) was investigated in patients with progressive renal disease requiring treatment for renal anemia with Epo. The subjects for the study were patients with renal diseases with serum creatinine concentration exceeding 2 mg/dl and a hematocrit (Ht) of less than 30%. During the run-in period, blood pressure was well controlled with an appropriate salt restricted diet and/or antihypertensive treatment. The patients were then given 6,000 IU of Epo once a week until the Ht rose by 5%. For the overall patient group, AGT gene polymorphism analysis revealed T235T (T/T) in 31 cases (61%), M235T (M/T) in 19 cases (37%), and M235M (M/M) in 1 case (2%). In response to treatment with Epo, hypertension (defined as an increase in mean blood pressure greater than 10 mmHg) was found in 11 cases (22%), all of who carried the homozygous T allele (T/T). On the other hand, the frequency of T/T in patients who did not develop hypertension was 50% (T/T:T/M=20:19 cases), indicating a significant difference (p=0.003 by Chi-square). Variables estimated to be associated with Epo-induced hypertension were the T allele, gender (male), and the degree of increase in Ht, in descending order. Our preliminary research indicates that individuals who carry two copies of the T allele, i.e., who are homozygous for T, are highly susceptible to development of hypertension when subjected to Epo. These results suggest that the AGT T235 variant may be the primary gene responsible for the development of Epo-induced hypertension.

Circulating adrenomedullin in erythrocopietin-induced hypertension.

Levels of adrenomedullin (AM) have been shown to be elevated in hypertension and chronic renal failure, suggesting that AM plays a role in the pathogenesis of these diseases. The objective of the present study was to investigate whether circulating AM is involved in erythropoietin (Epo)-induced hypertension in patients with renal anemia due to progressive renal disease. Following treatment with 6,000 IU of Epo once a week, the hematocrit (Ht) rose significantly from 25.9+/-4.0 to 33.4+/-3.3% (n=54, p<0.001) with an overall rate of increase in Ht of 0.43+/-0.04%/week. In response to treatment with Epo, a rise in mean blood pressure of >10 mmHg (Epo-induced hypertension) was found in 22% (12/54 cases) of the patients enrolled. There was no difference in the rate of Ht increase between patients with and without Epo-induced hypertension. There was a significant positive correlation between mature AM and serum creatinine (Cr) concentration before treatment with Epo. However, no correlation was found between the plasma concentration of total AM and serum Cr concentration. Long-term treatment with Epo did not influence plasma concentration of either mature AM or total AM in patients developing hypertension during the study period. These results suggest that circulating AM may play a role in the progression of renal disease. However, the present study does not support the notion that circulating AM is associated with the pathogenesis of Epo-induced hypertension. It is too early yet to claim that there is no AM-mediated mechanism in Epo-induced hypertension.

Differential regulation of cation transport of vascular smooth muscle cells in a high glucose concentration milieu.

To gain new insights into the pathogenesis of diabetic angiopathy, the influence of high glucose concentration on cation transport of vascular smooth muscle cell (VSMC) membrane was investigated by measuring Na, K and Ca transport in serially passaged cultured VSMC. (1) Na-K pump activity, described as ouabain sensitive 86Rb uptake, and Na-K cotransport, described as bumetanide sensitive 86Rb washout of VSMC, grown in high glucose concentration medium (460 mg/dl), was lower than that grown in normal glucose concentration medium (100 mg/dl). A smaller 5-N,N-hexamethylene amiloride (HMA) sensitive 22Na uptake (Na-H antiport) in high glucose concentration medium. accounted for this difference. (2) 45Ca uptake was also smaller in VSMC cultured in high glucose concentration medium. However, the washout rate constant for 45Ca was comparable between high and normal glucose cultured VSMC. (3) Both intracellular concentration of Na and cytosolic free Ca concentration concentration ([Ca]i) of high glucose cultured VSMC were greater than normal glucose cultured VSMC. (4) Intracellular water volume based on the equilibrium distribution of 3-O-methyl-[14C]glucose was not different between normal and high glucose cultured VSMC. It is concluded that VSMC grown in high glucose concentration milieu manifests a decreased Na-K, and Ca transport in conjunction with an increase in intracellular concentration of Na and [Ca]i. These results suggest that high glucose, per se, may alter membrane permeability to cations, possibly leading to changes in VSMC contractility and/or proliferation. This abnormality seen in the diabetic state may closely link to the pathogenesis of diabetic angiopathy, thus as a result risking hypertension and vascular disease.

Tranexamic acid increases peritoneal ultrafiltration volume in patients on CAPD.

OBJECTIVE: The preservation of ultrafiltration (UF) capacity is crucial to maintaining long-term continuous ambulatory peritoneal dialysis (CAPD).The aim of the present study was to investigate whether the antiplasmin agent tranexamic acid (TNA) increases UF volume in CAPD patients. PATIENTS AND METHODS: Fifteen patients on CAPD, 5 with UF loss and 10 without UF loss, were recruited for the study. The effect of TNA was evaluated with respect to changes in UF volume, peritoneal permeability, peritoneal clearance, bradykinin (BK), and tissue plasminogen activator (tPA) concentration. SETTING: Dialysis unit of the Saiseikai Central Hospital. RESULTS: In patients with UF loss, 2 weeks of treatment with oral TNA produced a significant increase in UF volume in all subjects (5/5).TNA also produced a significant increase in peritoneal clearances of urea and creatinine (Cr). However, the peritoneal equilibration test (PET) revealed that TNA had no effect on dialysate/plasma (D/P) Cr, Kt/V, or the protein catabolic rate (PCR).TNA also had no effect on net glucose reabsorption. In contrast, significant decreases in BK and blood tPA concentrations in response to TNA treatment were noted. BK concentration in drainage fluid was also reduced. In the case of patients without UF loss,TNA produced an increase in UF volume in 70% (7/10). However, no differences were found in blood and drainage BK and tPA concentrations between theTNA treatment and nontreatment periods in these patients. A comparison of basal BK and tPA concentration showed that there were no differences in these parameters between patients with UF loss and those without loss of UF. Furthermore,TNA given intraperitoneally to a patient also produced a marked increase in UF volume. CONCLUSION: The present study suggests thatTNA enhances UF volume in patients both with and without UF loss. SinceTNA did not affect peritoneal permeability and glucose reabsorption, the mechanism by which TNA exerts an enhancing action on UF is largely unknown. We speculate that it may be associated with suppression of the BK and/or tPA system, at least in patients with UF loss.

True median cleft of the upper lip associated with three pedunculated club-shaped skin masses.

A rare case of true median cleft of the upper lip associated with three skin masses is reported. While 114 cases of median cleft of the upper lip have been reported, in our literature review we found only 1 case, reported by Sharma, in which the median cleft was associated with skin masses. The embryology of this case is also discussed.

Acute renal failure after binge drinking of alcohol and nonsteroidal antiinflammatory drug ingestion.

A case of reversible acute renal failure (ARF) following binge drinking together with the transient use of a nonsteroidal antiinflammatory drug (NSAID) is described. After binge drinking. the patient experienced hyperdipsia, and the volume of his urine decreased. Subsequently, he took an NSAID to relieve systemic joint pain associated with low grade fever, and then he had complete anuria. One day after taking the NSAID, he visited our hospital, and was found to have severe renal dysfunction accompanied by severe liver damage (blood urea nitrogen and creatinine concentrations were 57 and 5.4 mg/dl, respectively). The impaired renal function progressed over the first three hospital days, as reflected by an elevated creatinine concentration to 11.6 mg/dl. Nine treatment sessions of hemodialysis were, therefore, required to recover the loss of renal function. The present case suggests that binge drinking may be a potential risk factor for ARF in the presence of NSAIDs.

Rhabdomyolysis associated with bacteremia due to Streptococcus viridans.

A 25-year-old man was admitted with complaints of fever and macrohematuria. Laboratory tests showed a substantial increase in serum creatine phosphokinase and creatinine in association with myoglobinuria and proteinuria. Blood culture grew Streptococcus salivarius and Streptococcus oralis. Findings of renal biopsy were compatible with IgA nephropathy. The glomeruli had a mild mesangial proliferation without crescentic lesions. Changes of the interstitium and tubules were not evident. The clinical course and laboratory results strongly suggested a possible link between Streptococcus salivarius/oralis infection, and rhabdomyolysis. Rhabdomyolysis is rarely seen as a complication of bacterial infection, and the present case emphasizes the importance of suspecting bacteremia due to Streptococcus salivarius/oralis in the presence of rhabdomyolysis.

Malignant insulinoma with extensive liver metastases presenting as disturbance of consciousness.

A 56-year-old man was referred to our hospital for evaluation of episodic disturbance of consciousness. Hypoglycemic symptoms were noted and Whipple's triad was satisfied. The 75 g OGTT and the glucagon test revealed a high baseline insulin level and hyperreactivity to glucagon. A pancreatic tumor and liver metastases were found by abdominal computed tomography (CT). Based on the finding of liver biopsy, the final diagnosis was malignant insulinoma with liver metastasis. He selected conservative treatment and no hypoglycemic crisis has occurred for one year since discharge. Early diagnosis and long-term follow-up is necessary since this tumor is slow growing.

Partial deficiency of hypoxanthine-guanine phosphoribosyltransferase manifesting as acute renal damage.

A 32-year-old man who had had frequent gouty arthritis over the past 17 years, was admitted for acute renal failure. Acute renal failure was improved rapidly after medication was resumed and the patient was sufficiently hydrated. The hypoxanthine-guanine phosphoribosyltransferase (HPRT) activity in the patient had been reduced to about 30% of the normal control. Therefore we considered that this patient suffered from a partial deficiency of HPRT. A point mutation of HPRT gene 68G (guanine) to T (thymine) was detected. This is a mutation that has not been previously reported. Familial analysis indicated that his mother and sister were heterozygotes.

Intermittent outpatient based ECUM. A case report.

Extracorporeal Ultrafiltration Method (ECUM) could be used in patients with refractory congestive heart failure (CHF). We have encountered a 56-year-old woman with refractory congestive heart failure (CHF) (NYHA II-III) due to coronary artery disease, complicated by moderately advanced diabetic nephropathy (Cr = 2.4 mg/dl). Due to the non-responsiveness to medical treatments, she has begun receiving the intermittent ECUM once or twice a week on an outpatient basis. ECUM effectively reduced cardiac preload and temporarily relieved her intractable respiratory distress. Based on our present clinical experience, we propose that one could consider an outpatient based intermittent ECUM as one of the useful therapeutic modalities to ameliorate refractory CHF.

[Ambulatory blood pressure monitoring in hypertensive CAPD patients].

The periodic structure of 24-hour blood pressure variation(circadian rhythm of blood pressure by ambulatory blood pressure monitoring(ABPM) in hypertensive CAPD patients was investigated by a new method of analysis based upon the maximum entropy method(MEM). In addition, this method allows the adequacy of antihypertensive therapies to be evaluated in such patients. The results were as follows; 1) The frequency of non-dipper type hypertension was 88%(36/41 cases), and the remaining 12% (5/41) were dipper type hypertension patients. The rise in morning blood pressure(morning surge: MS) was noted in 64% of the former. 2) Night time systolic blood pressure(182 +/- 22 mmHg, n = 36) was higher in patients with non-dipper type hypertension than in those with the dipper type(151 +/- 17 mmHg, n = 5, p < 0.01). 3) The standardized level of systolic blood pressure(SLSBP) calculated by MEM analysis in patients with non-dipper type hypertension(177 +/- 7 mmHg) was comparable with that in those with dipper type hypertension(168 +/- 13 mmHg, ns). 4) Treatment with long-acting Ca antagonist alone significantly reduced both SLSBP and the area over the SLSBP from 188 +/- 18 mmHg to 160 +/- 7 mmHg(p < 0.01, n = 8), and area over the SLSBP from 2,735 +/- 340 mmHg.hr to 1,945 +/- 298 mmHg.hr(p < 0.01, n = 8). 5) In addition to long-acting Ca antagonist, administration of alpha 1-blocker given at bed time was significantly efficacious in reducing the rise in morning blood pressure, MS. The present study using MEM analysis of ABPM suggests that the blood pressure profile of hypertensive CAPD patients is characterized by a non-dipper type dominance and a frequent morning surge. Furthermore, the combined therapy with long-acting Ca antagonist and alpha 1-blocker was substantially effective both in reducing the overall blood pressure level, and in inhibiting the MS. This combined antihypertensive therapy may be potentially useful to prevent CAPD patients from the future development of cardiovascular complications.