Spontaneous remission of a solitary eosinophilic granuloma of the mandible after biopsy: a case report.
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Biopsy↗
Biomedical subjects
H Yoshida
Publications and source records attributed to H Yoshida.
Pulsed Doppler sonography for the diagnosis of strangulation in small bowel obstruction.
BACKGROUND/PURPOSE: This study was undertaken to assess the usefulness of pulsed Doppler sonography (PDS) for the detection of strangulation in small bowel obstruction by evaluating the hemodynamics in the superior mesenteric artery (SMA). METHODS: The authors performed PDS in 117 normal children: 22 children aged 0 to 1 months (group I), 27 children aged 1 to 12 months (group II), 36 children aged 1 to 6 years (group III), and 32 children aged 7 to 15 years (group IV). Patients included 25 with simple obstruction: 1 in group II, 10 in group III, and 14 in group IV; and 9 with strangulating obstruction: 2 in group I, 2 in group II, 3 in group III, and 2 in group IV. The authors measured the peak-systolic velocity, end-diastolic velocity (EDV), and mean average velocity and calculated the resistive index (RI). RESULTS: The authors observed both a significant decrease in the EDV and increase in the RI for the SMA in strangulating obstruction compared with simple obstruction. CONCLUSION: Analysis of the hemodynamics in the SMA using PDS is useful to differentiate strangulating obstruction from simple obstruction.
Adolescent↗
Pulsed Doppler sonography of the hilar renal artery: differentiation of obstructive from nonobstructive hydronephrosis in children.
BACKGROUND/PURPOSE: It is difficult to detect the arcuate or cortical renal arteries when performing pulsed Doppler sonography (PDS) for congenital hydronephrosis. This study was undergone to assess the usefulness of PDS of the hilar renal artery to differentiate obstructive from nonobstructive hydronephrosis. METHODS: The authors performed PDS of the hilar renal artery in 80 normal children: 20 aged 0 to 1 months (group I), 20 aged 1 to 12 months (group II), 20 aged 1 to 6 years (group III), and 20 aged 7 to 15 years (group IV). Based on diuretic renography findings, 22 kidneys from 19 children with a ureteropelvic junction (UPJ) stricture were divided into 7 dilated obstructed and 15 dilated nonobstructed kidneys. The peak-systolic velocity (PSV), end-diastolic velocity (EDV), mean average velocity (Vm) and the resistive index (RI = [PSV - EDV]/PSV) were measured at the hilar renal artery. RESULTS: There was a significant difference in the RI of the hilar renal artery between obstructive and nonobstructive hydronephrosis. CONCLUSION: A pulsed Doppler evaluation of the hilar renal artery is useful for detecting an obstructive UPJ stricture compared with assessing arcuate or cortical renal arteries.
Adolescent↗
Successful surgical treatment of two cases of congenital chylous ascites.
The authors report on 2 patients with congenital chylous ascites who underwent successful lymphatic duct ligation after a laparoscopic lymphoid dye test. Fetal ascites had been detected in both cases, and both babies were born with marked abdominal swelling. Given that conservative treatment by medium-chain triglyceride (MCT) milk and total parenteral nutrition (TPN) was ineffective, the authors elected to perform lymphatic duct ligation on the 95th postnatal day in the former case and on the 27th postnatal day in the latter case. Lipophilic dye was administered preoperatively both through oral and subcutaneous routes, and the peritoneal cavity was explored using laparoscopy. This laparoscopic lymphoid dye test precisely identified the area of chylous leakage, and the authors were able to repair the malformed lymphatic duct directly at laparotomy. Both postoperative courses have been favorable with no recurrence of symptoms. The lymphatic duct ligation should be considered in cases resistant to conservative treatment for over a month. The present laparoscopic lymphoid dye test is a novel and useful procedure that allows surgeons to identify the exact location of chylous leakage, and thus successfully ligate the lymphatic duct.
Chylous Ascites↗
Predictors for development of hyperuricemia: an 8-year longitudinal study in middle-aged Japanese men.
To identify the factors responsible for increases in serum uric acid (SUA), a cohort of 1,312 hyperuricemia-free (SUA < 7.5 mg/dL and no medication for hyperuricemia or hypertension) male office workers aged 30 to 52 years were examined annually for 8 successive years. Subjects who were found to have become hyperuricemic (SUA > or = 7.5 mg/dL) or who started medication for hyperuricemia during repeat surveys were defined as incidence cases. The SUA trend was also examined in 1,062 subjects for whom 9 consecutive SUA values were available and who did not start medication for hyperuricemia or hypertension during the observation period. Multivariate analyses, excluding the baseline SUA level as a factor in the Cox proportional-hazards model, indicated that age (negative), body mass index (BMI), log triglyceride level, hemoglobin A(1c) (HbA(1c)) level (negative), white blood cell count, and alcohol intake at study entry were significantly associated with the incidence of hyperuricemia. In the model including the baseline SUA level, baseline SUA level was the strongest factor for the incidence of hyperuricemia, and BMI, white blood cell count, and alcohol intake at study entry remained as independent factors. From stepwise linear regression analyses for SUA slope, excluding the baseline SUA level as a factor, significant correlates with SUA slope were, in order of their relative importance, slopes of BMI, HbA(1c) (negative), blood urea nitrogen, log triglyceride level, total protein, and baseline levels of hematocrit (negative), white blood cells, and HbA(1c) (negative). In stepwise linear regression analyses, including the baseline SUA level as a factor, SUA level (negative) and alcohol intake at study entry emerged as significant factors for SUA slope. The cumulative percentage of variation for SUA slope was 25.6%. In conclusion, obesity, alcohol intake, and multimetabolic disorders were determined to be independent predictors for the development of hyperuricemia. In addition, the white blood cell level may be a contributory factor.
Adult↗
Blunted peripheral vasodilatory response is a hallmark of progressive deterioration in mild to moderate congestive heart failure.
BACKGROUND: Several reports have shown that dilatory response to acetylcholine (ACh) and nitroprusside (SNP) is blunted in the limb vasculature in patients with congestive heart failure (CHF). However, it is not yet known whether this vascular dysfunction is related to clinical outcome. We have examined the relationship between peripheral vasodilatory response and prognosis of CHF. METHODS AND RESULTS: A total of 46 patients with mild to moderate CHF were enrolled (mean age 56 years). Changes in forearm blood flow (FBF) during intra-arterial infusion of ACh and SNP were determined by plethysmography. FBF changes above baseline for each dose were cumulated and used as an index of endothelium-dependent (ACh) response and endothelium-independent (SNP) response, respectively. During the follow-up period (mean 32 months), 9 patients were admitted to the hospital for treatment of worsening refractory CHF, and 6 patients died suddenly or developed life-threatening arrhythmia. By Kaplan-Meier analysis, when all cardiac events were included, no significant differences were observed between any levels of vascular response in terms of prognosis. However, when deterioration events were analyzed separately, patients with SNP responses below the median (7.4 mL/min/dL) had significantly higher rates of hospital admission caused by worsening CHF than those with above the median responses (P <.05). This relationship was not found between ACh response and clinical outcome. By Cox multivariate analysis, blunted vasodilatory response to SNP was a significant predictor of worsening CHF (chi(2) = 3.95; P <.05). CONCLUSION: This study has shown that patients with mild to moderate CHF showing a blunted vascular response to SNP rather than ACh were admitted to the hospital more frequently because of deterioration of CHF. This finding suggests that changes in vascular smooth muscle and/or vascular structure in the peripheral vasculature may be a critical element in the worsening of CHF.
Acetylcholine↗
Systemic and renal effects of atrial natriuretic peptide in patients with heart failure treated with angiotensin-converting enzyme inhibitor or in acute saline solution loading.
BACKGROUND: Our purpose was to study the effects of atrial natriuretic peptide (ANP) on cardiorenal functions when it is used to manage patients with heart failure who are receiving an angiotensin-converting enzyme inhibitor (ACEi) or in acute saline solution loading. METHODS: Seventeen patients with mild to moderate heart failure were entered into protocol 1 or 2. Protocol 1 was ANP (30 ng/kg/min) infused before and after treatment with ACEi (n = 9). Protocol 2 was acute saline loading with or without coadministration of ANP (n = 8). In both protocols cardiorenal hemodynamics and urinary sodium excretion were assessed before and after each intervention. RESULTS: Protocol 1: Although ANP infusion significantly increased urinary sodium excretion to a similar extent before and after ACEi treatment, the infusion increased the glomerular filtration rate (75 +/- 16 --> 82 +/- 15 mL/min, P <.05) and renal blood flow (390 +/- 123 --> 438 +/- 140 mL/min, P <.05) only before ACEi treatment. Protocol 2: Acute saline solution loading decreased plasma renin activity (P <.05) but did not affect ANP level. Coadministration of ANP with saline solution load enhanced the increase of urinary sodium excretion (75% +/- 34% increase) compared with the acute saline solution load alone (49% +/- 33% increase) (P <.05) but had no affect on renal hemodynamics. CONCLUSIONS: When ANP is used in patients with mild to moderate heart failure who are on combined ACEi treatment or in acute saline solution loading, the vasodilatory effect of ANP is blunted while the natriuretic effect of ANP is preserved. The renin-angiotensin system seems to modulate the vasodilatory effect of ANP.
Adult↗
Clarithromycin-based triple therapy for non-resistant Helicobacter pylori infection. How long should it be given?
BACKGROUND: We have previously reported mixed infection with wild-type (sensitive) and mutant (resistant) Helicobacter pylori strains using a PCR-based preferential homo-duplex formation assay (PCR-PHFA) to detect gene mutations associated with clarithromycin resistance. Half of the cases with mixed infection were determined as sensitive by conventional MIC assessment and yet failed to respond to clarithromycin-based therapy. The aim of this study is to assess the efficacy of clarithromycin-based triple therapy in patients infected exclusively with wild-type strains as determined by PCR-PHFA. METHODS: Ninety patients who had pure wild-type H. pylori infection were randomly assigned to receive clarithromycin (200 mg b.i.d.), amoxicillin (500 mg q.i.d.) and lansoprazole (30 mg b.i.d.) for either 5 days or 7 days (n = 48 and n = 42, respectively). The outcome of eradication was assessed by [13C] urea breath test. RESULTS: Eradication was achieved in 36/48 (75%) versus 39/42 (93%) by intention-to-treat analysis (P = 0.02), and in 36/45 (80%) versus 39/40 (98%) by per protocol analysis (P = 0.01), for the 5-day and 7-day protocols, respectively. Compliance and the incidence of untoward effects were similar in both groups. CONCLUSIONS: Seven-day administration is necessary and sufficient for the triple therapy with clarithromycin, amoxicillin and lansoprazole in patients with pure wild-type H. pylori infection.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Cilazapril prevents cardiac hypertrophy and postischemic myocardial dysfunction in hyperthyroid rats.
We evaluated the effects of hyperthyroidism on cardiac structural changes and postischemic myocardial function, and also studied how an angiotensin-converting enzyme (ACE) inhibitor, cilazapril, can alter these changes. Hyperthyroidism was induced by daily intraperitoneal injection of thyroxine (T4) (600 microg/kg) with or without cilazapril (10 mg/kg per day, orally), and control rats were given by vehicle. After 2 weeks of treatment, T4-treated rats showed increases in blood pressure and heart weight to body weight ratio (HW:BW). Cilazapril decreased blood pressure to control values and reduced HW:BW. In the isolated working heart preparation, T4-treated rats showed a poor postischemic recovery of left ventricular pressure-rate product (14% of baseline at 30 minutes of reperfusion vs. vehicle 85%) and cardiac work (6% vs. 71%). Cilazapril recovered both values to 49% and 43%. Propranolol (500 mg/L in drinking water) decreased blood pressure to the same extent as cilazapril in hyperthyroid rats, but changed neither HW:BW nor the postischemic myocardial dysfunction. Percent recovery of cardiac work was inversely well correlated with HW:BW (R2 = 0.998, p < 0.001). Results indicate that T4-induced cardiac hypertrophy enhances postischemic cardiac dysfunction. Results also indicate renin-angiotensin system (RAS), but not sympathetic nerve activation, is involved in cardiac hypertrophy and postischemic myocardial dysfunction in hyperthyroid rats.
Adrenergic beta-Antagonists↗
Effects of lansoprazole, clarithromycin and pH gradient on uptake of [14C]amoxycillin into rat gastric tissue.
The effect of lansoprazole and clarithromycin on the uptake of [(14)C]amoxycillin into rat gastric tissue was investigated. After oral administration of [(14)C]amoxycillin, the levels of radioactivity in gastrointestinal tissue were two to 15 times higher than those in plasma. The level of radioactivity in glandular stomach was significantly higher when lansoprazole and [(14)C]amoxycillin were administered together. After intravenous administration of [(14)C]amoxycillin, there was less radioactivity in gastric tissue than after oral administration, and co-administration of lansoprazole and clarithromycin had no obvious effect. The gastric emptying rate of [(14)C]amoxycillin was not apparently affected by the co-administration of lansoprazole and clarithromycin. In vitro uptake of [(14)C]amoxycillin into gastric tissue depended on the pH, with uptake at pH 7.4 being four times greater than that at pH 4.0. The apparent synergic effects of lansoprazole are due to enhanced penetration of amoxycillin in gastric mucus and tissue by increasing intragastric pH and play an important role in the eradication of H. pylori.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Localization of [14C]amoxicillin in rat gastric tissue when administered with lansoprazole and clarithromycin.
The gastric mucosal distribution of [14C]amoxicillin when administered to rats with or without lansoprazole and clarithromycin was investigated. After oral administration, the amount found in the gastric mucosa was higher than after iv administration. Co-administration of lansoprazole and clarithromycin had no apparent effect on the distribution pattern of [14C]amoxicillin within the deeper stomach layers. About 50-60% of the radioactivity in the gastric tissue was present in the mucosal layer, irrespective of the route of administration. Microautoradiograms of the gastric mucosa indicated that [14C]amoxicillin was distributed in both the mucous layer and surface epithelial cells following oral administration. [14C]amoxicillin was secreted mainly by surface epithelial cells after iv administration, although only in small quantities.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Fatty acids enhance GRO/CINC-1 and interleukin-6 production in rat intestinal epithelial cells.
Intestinal mucosal immunity is modulated by cytokine release from intestinal cells, but little is known about the relation between nutrient absorption and cytokine release. In this study, we examined how exposure to fatty acids affects the production of growth-regulated oncogene/cytokine-induced neutrophil chemoattractant-1 (GRO/CINC-1) and interleukin (IL)-6 in rat intestinal epithelial cells (IEC). The long-chain fatty acids, oleic, linoleic and arachidonic acids, and the middle-chain fatty acid octanoic acid were administered to subconfluent cultures of IEC-6 cells alone, or in combination with IL-1beta and transforming growth factor (TGF)-beta. The GRO/CINC-1 and IL-6 concentrations in culture media were determined by sandwich enzyme immunoassay. In epithelial cells, GRO/CINC-1 and IL-6 mRNA expression were examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and mitogen-activated protein kinase (MAPK) activities determined by immunoblotting. Administration of long-chain fatty acids significantly increased the GRO/CINC-1 and IL-6 secretion into culture media, and this secretion was markedly increased (P < 0.05) in the presence of IL-1beta or TGF-beta. Octanoic acid had no effect on GRO/CINC-1 or IL-6 production. Furthermore, treatment with long-chain fatty acids significantly enhanced the GRO/CINC-1 and IL-6 expression that was induced by IL-1beta or TGF-beta. MAPK activity was significantly enhanced by treatment with long-chain fatty acids. Inhibitors of phospholipase C, protein kinase C or MAPK significantly reduced the fatty acid-induced increase in GRO/CINC-1 secretion, whereas a calcium/calmodulin inhibitor did not attenuate the secretion. These results suggest that long-chain fatty acids enhance cytokine release under conditions of inflammatory stimulation in the intestinal mucosa.
Animals↗
Macrophage and platelet-infiltrated glomerulonephritis with interstitial angiofollicular hyperplasia in a patient with POEMS syndrome.
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Blood Platelets↗
Caspase-independent cell death and mitochondrial disruptions observed in the Apaf1-deficient cells.
Apaf1 is a critical molecule in the mitochondria-dependent apoptotic pathway. Here we show that Apaf1-deficient embryonic fibroblasts died at a later phase of apoptotic induction, although these cells were resistant to various apoptotic stimulants at an early phase. Neither caspase 3 activation nor nuclear condensation was observed during this cell death of Apaf1-deficient cells. Electron microscopic examination revealed that death in response to apoptotic stimulation resembled necrosis in that nuclei were round and swollen with low electron density. Necrosis-like cell death was also observed in wild-type cells treated with z-VAD-fmk. Mitochondria were not only morphologically abnormal but functionally affected, since mitochondrial transmembrane potential (DeltaPsim) was lost even in cells with intact plasma membrane integrity. These mitochondrial alterations were also observed in the wild-type cells dying of apoptosis. Combined, these data suggest that cells without caspase activation, such as Apaf1-deficient cells or cells treated with caspase inhibitors, die of necrosis-like cell death with mitochondrial damage in response to "apoptotic stimulation."
Amino Acid Chloromethyl Ketones↗
Three-dimensional structural model analysis of the binding site of lithocholic acid, an inhibitor of DNA polymerase beta and DNA topoisomerase II.
The molecular action of lithocholic acid (LCA), a selective inhibitor of mammalian DNA polymerase beta (pol beta), was investigated. We found that LCA could also strongly inhibit the activity of human DNA topoisomerase II (topo II). No other DNA metabolic enzymes tested were affected by LCA. Therefore, LCA should be classified as an inhibitor of both pol beta and topo II. Here, we report the molecular interaction of LCA with pol beta and topo II. By three-dimensional structural model analysis and by comparison with the spatial positioning of specific amino acids binding to LCA on pol beta (Lys60, Leu77, and Thr79), we obtained supplementary information that allowed us to build a structural model of topo II. Modeling analysis revealed that the LCA-interaction interface in both enzymes has a pocket comprised of three amino acids in common, which binds to the LCA molecule. In topo II, the three amino acid residues were Lys720, Leu760, and Thr791. These results suggested that the LCA binding domains of pol beta and topo II are three-dimensionally very similar.
African Swine Fever Virus↗
Orientation and osteoarthritis of the lumbar facet joint.
Several studies have shown an association between sagittal orientation of the facet joint and degenerative spondylolisthesis. There is currently no information available on the association between orientation of the facet joint and osteoarthritis. This study examined the association between orientation and osteoarthritis of the lumbar facet joints. One hundred eleven consecutive patients underwent plain radiography and magnetic resonance imaging. These patients were divided into two groups: No Degenerative Spondylolisthesis Group (98 patients) and Degenerative Spondylolisthesis Group (13 patients). In the No Degenerative Spondylolisthesis Group, segments with higher grades of osteoarthritis showed more sagittal orientation of the facetjoints at the L3-L4 and L4-L5 levels. The facet joint was oriented significantly more sagittally in the Degenerative Spondylolisthesis Group than in the No Degenerative Spondylolisthesis Group at the L4-L5 and L5-S1 levels. The severity of facet joint osteoarthritis was significantly higher in the Degenerative Spondylolisthesis Group than in the No Degenerative Spondylolisthesis Group at the L3-L4, L4-L5, and L5-S1 levels. A significant association was found between sagittal orientation and osteoarthritis of the lumbar facet joints, even in patients without degenerative spondylolisthesis. Facet joint osteoarthritis, rather than spondylolisthesis, is the pathoanatomic feature that is associated with sagittal orientation of the facet joints in patients with degenerative spondylolisthesis.
Aged↗
Intraoperative prostaglandin E1 improves antimicrobial and inflammatory responses in alveolar immune cells.
OBJECTIVE: Anesthesia and surgery decrease antimicrobial and increase proinflammatory functions of alveolar immune cells. Thus, anti-inflammatory agents that do not further suppress antimicrobial functions are required. We tested the hypothesis that intraoperative prostaglandin E1 (PGE1) suppresses proinflammatory responses and prevents the reduction in antimicrobial responses of alveolar immune cells. DESIGN: Prospective, randomized, controlled, double-blind study. SETTING: University hospital. PATIENTS: A total of 40 patients undergoing elective orthopedic surgery under propofol/fentanyl anesthesia. INTERVENTION: In double-blind fashion, the patients received PGE1 from the beginning to the end of surgery (PGE1 group, n = 20) or nothing (control group, n = 20). METHODS AND MAIN RESULTS: Alveolar immune cells were harvested by bronchoalveolar lavage immediately after induction of anesthesia; 2, 4, and 6 hrs after induction of anesthesia; and at the end of surgery. We measured opsonized and nonopsonized phagocytosis. Microbicidal activity was evaluated to directly kill Listeria monocytogenes in alveolar macrophages. Finally, we determined the expression of proinflammatory cytokines including interleukin (IL)-1beta, IL-8, interferon-gamma, and tumor necrosis factor-alpha, and that of anti-inflammatory cytokines (IL-4 and IL-10) by semiquantitative polymerase chain reaction. Nonopsonized and opsonized phagocytosis and microbicidal activity of alveolar macrophages decreased and the expression of genes for all pro- and anti-inflammatory cytokines increased significantly over time in both groups. Starting 2-4 hrs after induction of anesthesia, the increases in gene expression of proinflammatory cytokines were 1.5-3 times smaller in the PGE1 than in the control group. Starting 6 hrs after anesthesia, the increase in gene expression of IL-10 was 1.5-3 times greater in the PGE1 than in the control group. Intraoperative decreases in phagocytic and microbial activities were the same in the two groups. CONCLUSION: Intraoperative PGE1 not only suppressed proinflammatory responses, but also protected antimicrobial functions of alveolar macrophages, possibly because PGE1 is mostly inactivated in the pulmonary intravascular space. Our results suggest that intraoperative PGE1 protects the pulmonary immune defense in alveolar immune cells.
Adult↗
Alcohol consumption and risk for hypertension in middle-aged Japanese men.
OBJECTIVE: To investigate the association of alcohol intake with development of hypertension. DESIGN: Longitudinal study (followed from 1990 to 1999). SETTING: Work site in Osaka, Japan. PARTICIPANTS: Japanese male office workers (n = 1,310) hypertension-free, with systolic blood pressure (SBP) less than 140 mmHg, diastolic blood pressure (DBP) less than 90 mmHg, no medication for hypertension, and no past history of hypertension, 30 to 59 years of age at study entry. MAIN OUTCOME MEASURE: Incidence of hypertension. RESULTS: After controlling for potential predictors of hypertension, the relative risk for hypertension (SBP 140 mmHg or greater and/or DBP 90 mmHg or greater or receipt of antihypertensive medication) compared with non-drinkers was 1.52 [95% confidence interval (CI), 1.05 to 2.19] for persons who drank 0.1 to 22.9 g/day of ethanol, 1.81 (95% CI, 1.29 to 2.54) for those who drank 23.0 to 45.9 g/day of ethanol, 2.12 (95% CI, 1.53 to 2.94) for those who drank 46.0 to 68.9 g/day of ethanol, and 2.48 (95% CI, 1.75 to 3.52) for those who drank > or = 69.0 g/day of ethanol (for trend, P < 0.001). The relative risk for hypertension in current drinkers versus non-drinkers was stronger among men with a body mass index (BMI) less than 24.2 kg/m2 than among men with a BMI 24.2 kg/m2 or more, although the absolute risk was greater in more obese men. CONCLUSIONS: The risk for hypertension increased in a dose-dependent manner as alcohol intake increased in middle-aged Japanese men. The increased relative risk for hypertension associated with alcohol was more pronounced in leaner men.
Adult↗