Hypophosphatemia and encephalopathy in alcoholics.
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Publications and source records attributed to N Nagata.
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In order to observe the reaction of cochlear blood flow (CBF) to trimetaphan (TMP)-induced hypotension, CBF was measured with laser-Doppler flowmetry in 7 human subjects during general anaesthesia for middle ear surgery. All subjects showed a decrease in mean arterial pressure (MAP) during intravenous infusion of TMP, followed by a gradual return to the baseline level after termination of the infusion. The CBF generally followed the MAP changes with the same pattern. Three of the seven subjects demonstrated a CBF change larger than the maximum MAP change, indicating the lack of a local autoregulatory mechanism in CBF. On the other hand, CBF changes were smaller in magnitude than the maximum change in MAP for the rest of the subjects, suggesting an autoregulatory mechanism in CBF. However, since the audiograms from these subjects indicated profound damage along the cochlear basal turn probably due to middle ear inflammation, concomitant vascular damage in this region offers another possible explanation for the inappropriate CBF changes. The present observations may also suggest that deliberately TMP-induced hypotension has a potentially harmful effect on CBF during otological surgery that attempts to preserve or improve hearing.
The novel uracil analog, 6-chloro-5-(2-propenyl)uracil (TI90), inhibited the growth of myeloid leukemia cells and induced morphologic and functional differentiation of the cells. Although TI90 was a weak inducer of differentiation, it greatly enhanced the growth inhibition and differentiation of the leukemia cells previously induced by 1alpha,25-dihydroxyvitamin D3 (VD3) or all-trans retinoic acid (ATRA). TI90 cooperated with VD3 much more effectively than with ATRA in inhibiting cell growth and inducing differentiation. It also decreased the effective concentration of VD3 to the 10(-10) M level. On the other hand, there was no significant synergy between VD3 and the other uracil analogs. TI90 did not affect VD3 metabolism or the number and affinity of VD3 receptors (VDR) in HL-60 cells. Signals from VD3 are predominantly mediated by VDR and the ligand-activated binding of VDR to vitamin D-responsive element (VDRE) as a heterodimer with the retinoid X receptor (RXR). According to the results of a gel shift assay, TI90 enhanced the intensity of the retarded band with synthetic VDRE oligomer in the presence of VD3, suggesting that TI90 increases the number of phosphorylated receptors by inhibiting phosphatase activity, and also stimulates the formation of a functional complex of VDR with RXR.
A 7-year-old boy was admitted for RVOT restenosis. The patient was born following an unremarkable pregnancy and delivery. He was carried out Jatene's procedure for TGA at 23rd day after birth. At 19 month of age, he was removed pulmonary stenosis using patch angioplasty with mono cusp. When he was 6 year of age, the onset of edem, ascites and hepatomegaly were pointed out. At 7 year of age, he was admitted for edema, hypoproteinemia and protein loosing enteropatchy. After he was treated medical therapy, cardiac catheterization showed markedly right atrial and right ventricular hypertension and ventricular septal defect (VSD). Cine angiography suggested the right ventricular outflow tract stenosis, pulmonary valve and tricuspid valve insufficiency. On August 1, 1996, the patient underwent surgical repair: direct closure of VSD, aortic homograft (20mm) replacement for RVOT stenosis and tricuspid valve annuloplasty by DeVega's procedure. Postoperative course was uneventful. At 23rd postoperative day, cardiac catheterization and cine angiography showed no problems. He was not treated with anticoagulation.
We report six cases of primary pulmonary lymphoma in which a gene-rearranged band was shown by Southern blot analysis of transbronchial or surgical biopsy specimens. The cases were 3 mens and 4 women with an average age of 59.6, who had abnormal pulmonary shadows on chest X-ray. Two cases had Sjögren's syndrome and one case had monoclonal gammopathy (IgM-lambda type). Histopathologic and immunologic examination revealed diffuse infiltration of small lymphocytes (B-cell type) in all cases, and histological features of lymphoepithelial lesion or lympho-cytic interstitial pneumonia (LIP) in three cases. CT revealed an ill-defined margin, air-space consolidation, and air-bronchogram in all cases. A CT-angiogram sign was apparent in 2 cases. In all cases, Southern blot analysis of the tissue obtained from transbronchial or surgical biopsy revealed a gene re-arranged band, supporting the diagnosis of primary pulmonary lymphoma. We infer that an ill-defined margin, air-bronchogram and air space consolidation on CT were associated with the histopathological features of primary pulmonary lymphoma.
After right heart bypass operation, dopamine was continuously infused at 5 micrograms/kg/min. The patients had a stable hemodynamic status but relatively low SvO2, low urine output and peripheral insufficiency. Amrinone was continuously infused at 10 micrograms/kg/min in 5 patients (Group A), or milrinone was continuously infused at 0.5 microgram/kg/min in 5 patients (Group M). After infusion of amrinone or milrinone, arterial blood pressure relatively decreased and heart rate relatively increased. But heart work index did not increased. SvO2 relatively increased. Mean pulmonary artery pressure relatively decreased. The administration of amrinone (Group A) produced relatively thrombocytopenia compared with milrinone (Group M). Two patients had supraventricular arrhythmia in Group A. A patient had ventricular arrhythmia and another patient supraventicular arrhythmia. These patients treated using temporary antiarrhythmia drug or temporary pacing. When the patients discharged, they recovered the normal sinus rhythm. In conclusion, after right heart bypass operation in infants, infusion of amrinone or milrinone appears to be effective and safe combining with dopamine.
A 48-year-old man was admitted because of persistent dry cough for six months. He had been a smoker for 25 years, averaging a pack a day, and demonstrated clubbing of the fingers. Basilar fine crackles were observed in both lung fields. Chest X-ray films on admission showed diffuse reticulonodular shadows. Chest computed tomograms showed low-attenuation areas mainly in the center of the upper lung field, and ground-glass opacity, air bronchiolograms, and perivascular interstitial thickening of the peripheral vessels mostly in the lower field. A Gascintigram disclosed mild accumulation in both lungs. A transbronchial lung biopsy specimen did not reveal special features. However, a biopsy specimen obtained by thoracoscopy showed evidence of respiratory bronchiolitis, with a mononuclear inflammatory process involving respiratory bronchioles and adjacent air space, associated with mild fibrous thickening of the peribronchiolar interstitium and surrounding alveoli septa. These findings suggested that the patient had respiratory bronchiolitis-associated interstitial lung disease, the second case to be reported in Japan.
Differanisole A, 3,5-dichloro-2-hydroxy-4-methoxy-6-n-propylbenzoic acid, inhibited growth of human myeloid leukemia cells. The compound induced G1 arrest and granulocytic differentiation of HL-60 cells, although the differentiation-inducing effect was modest. Differanisole A and 9-cis retinoic acid (9cisRA) synergistically inhibited the growth and induced functional and morphologic differentiation of HL-60 and NB4 cells, whereas the combined treatment with differanisole A and all-trans retinoic acid or 1alpha,25-dihydroxyvitamin D3 was less effective. Similar results were obtained in primary culture of leukemia cells from a patient with acute promyelocytic leukemia. The synergistic effect on growth inhibition and induction of differentiation required simultaneous treatment with differanisole A and 9cisRA. Differanisole A and an RXR-specific ligand (Ro47-5944) cooperatively inhibited the cell growth, while the combined effect of differanisole A and an RAR-specific ligand Am80 was just additive. Differanisole A in combination with 9cisRA may have implications for therapy of acute promyelocytic leukemia patients.
Excitotoxicity secondary to the loss of glutamate transporters (GluT) has been proposed as a possible pathogenetic mechanism for neuronal degeneration in amyotrophic lateral sclerosis. We therefore investigated whether prolonged in vivo pharmacologic inhibition of GluT would result in neuronal damage in the rat. DL-Threo-beta-hydroxyaspartate (THA), a potent GluT inhibitor, and glutamate were continuously infused into the rat spinal subarachnoid space by using a mini-osmotic pump. Animals that received both THA and glutamate, but not those received either singly, displayed tail paralysis with or without hind-limb paralysis and urinary incontinence after the third postoperative day. Pathologically, symptomatic animals exhibited neuronal loss with a variable extent of gliosis preferentially involving the dorsal horn of the lumbosacral cord. In the rostral spinal segments adjacent to those regions of intense pathologic changes, small neurons in the dorsal horn were selectively destroyed, a pattern similar to the late-onset neuronal damage induced by continuous intrathecal administration of 1-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) [R. Nakamura et al., Brain Res. 654 (1994) 279-285]. These behavioral and pathologic changes were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), suggesting that pharmacologic blockade of GluT causes selective neuronal damage in vivo by AMPA receptor activation.
A 47-year-old man experienced multifocal mononeuropathy and putative ganglionopathy associated with influenza B infection, characterized by aching and dysesthesia in the right arm and left leg with normal deep sense. He displayed muscle atrophy in the affected limbs, which might have resulted from local myositis or a disorder similar to neuralgic amyotrophy. Sural nerve biopsy revealed a severe loss of unmyelinated and thinly myelinated fibres, consistent with a small fibre neuropathy, without evidence of angiopathy or inflammation. We could not detect any other cause of the neuropathy except influenza B. In this case, it may be inferred that small-diameter neurons in the dorsal root ganglia and thinly- or nonmyelinated fibres were selectively involved through a post-infectious immune process. To our knowledge, small fibre neuropathy following influenza B has never been reported.
We examined the mechanism of the inflammatory response induced by topical application of mustard oil (0.5-20.0%/20 microliters per ear) to the mouse ear compared to that of the response to capsaicin. The dose-dependent increases in plasma extravasation and ear thickness reached a maximum at approximately 30 min after mustard oil application. Topical pretreatment of ears with capsaicin (250 micrograms/ear) diminished mustard oil-induced plasma extravasation for up to day 7 but not at day 14 after treatment. However, desensitization of the exudative response was not evoked by reapplication of mustard oil to ears. The inflammatory response to mustard oil did not differ between the ears of mast cell-deficient mice and those of the congenic normal mice. Mustard oil-induced plasma extravasation was unaffected by pretreatment with histamine H1 and 5-HT2 receptor antagonists and the capsaicin-functional inhibitor, ruthenium red, which inhibit capsaicin-induced ear oedema. The endopeptidase inhibitor, phosphoramidon, enhanced the ability of mustard oil to increase dye leakage. The tachykinin NK1 receptor antagonist, SR 140333 ((S)1-[2-[3-(3,4-dichlorophenyl)-1-(3-isopropoxyphenylacetyl)pi peridin-3-yl]ethyl]-4-phenyl-1-azoniabicyclo[2.2.2.]octane, chloride), not only inhibited mustard oil-induced plasma extravasation but also blocked the enhancement by phosphoramidon of the response to mustard oil. In contrast, the tachykinin NK2 receptor antagonist, SR 48968 ((S)-N-methyl-N[4-(4-acetylamino-4-phenylpiperidino)-2-(3,4,- dichlorophenyl)butyl]benzamide), and the tachykinin NK3 receptor antagonist, SR 142801 ((S)-(N)-(1-(3-(1-benzoyl-3-(3,4-dichlorophenyl)piperidin-3-yl)pro pyl)-4- phenylpiperidin-4-yl)-N-methylacetamide), had no effect on plasma extravasation. The present results demonstrated that mustard oil induces mouse skin inflammation through a mechanism different from that for capsaicin. Mediators such as histamine and 5-HT from mast cells appear to be minor factors in the response to mustard oil. In addition, evidence supports the assumption that the tachykinin NK1 receptor is involved in this model.
The clinicopathological features and operative results were analyzed in 21 patients undergoing an operation for cancer of the remnant stomach between 1979 and 1997. The twenty-one patients were divided into two groups: Group A; n = 9: who had undergone a gastrectomy for benign gastric disease, Group B; n = 12: who had undergone the same operation for gastric cancer. In Group A, the interval between the first gastrectomy and the second was longer than in Group B. In both groups, a large number of advanced cancers (n = 16, 76.2%) and undifferentiated carcinomas (n = 15, 71.4%) were seen. Five-year-survival rates in Group A and Group B were 23.7%, 19.0%, respectively. The incidence of gastric stump cancer following partial gastrectomy was 80% in the patients on whom Billroth II reconstruction had been performed after gastrectomy. It is suggested that the residual stomach in the Billroth II reconstruction patients is susceptible to cancer development. Consideration of the reconstruction method and a systemic follow-up is needed to improve a prognosis.
OBJECTIVE: To clarify the clinical features of and cardiotocographic findings for premature infants with antenatal periventricular leukomalacia (PVL). METHODS: Antenatal PVL was judged to be present if a cyst greater than 3 mm in largest diameter was detected in the periventricular region by the 14th day of life on cranial ultrasonography. The clinical features of and cardiotocographic findings for 12 premature infants with antenatal PVL born within 1 year were compared with those of 12 infants chosen as control group matched in gestational age at birth from the premature infants without antenatal PVL born within the study period. RESULTS: Abnormalities of the umbilical cord such as coiling, excessive torsion and membrane insertion were observed more frequently for infants with antenatal PVL (58.3%) than for control infants (16.7%) (P<0.05). Frequent moderate variable deceleration on the fetal cardiogram was also observed more frequently for infants with antenatal PVL (80.0%) than for control infants (27.3%) (P<0.05). CONCLUSION: Abnormalities of the umbilical cord and frequent moderate variable deceleration on fetal cardiotocogram appear to be causes of antenatal PVL in premature infants.
Most reports of MRI in Wilson's disease have been of abnormal low-signal lesions on T1-weighted images and high signal intensity on T2-weighted images. In contrast, we report three patients who had high-signal lesions in the globus pallidus on T1-weighted images, a finding seen in patients with portal-systemic encephalopathy. The possible causes include the paramagnetic effect of copper or iron and accumulation of Alzheimer type II glial cells.
Fractional esterification rate of cholesterol in high density lipoprotein (HDL) (FER[HDL]) can predict the size distribution and physicochemical characteristics of HDL in plasma. In the present study, we investigated the correlation of FER(HDL) with the particle size of low density lipoprotein (LDL) (LDL-size) in 111 patients (81 males and 30 females) with coronary heart disease (CHD). The correlations of FER(HDL) and LDL-size with conventional lipid and lipoprotein parameters were also studied. FER(HDL) was closely associated with LDL-size (males: r = -0.618, females: r = -0.629, P < 0.001). Plasma levels of TG, HDL-cholesterol (HDL-C), HDL2-cholesterol (HDL2-C) and apo B were also associated with LDL-size in male CHD patients (r = -0.534, 0.314, 0.358, and -0.482, P < 0.01 or 0.001), while plasma levels of TG and apo B were associated with LDL-size in female patients (r = -0.350 and -0.348, P < 0.05). In a stepwise multiple regression analysis, FER(HDL) alone accounted for 38 and 40% of the variability in LDL-size in male and female CHD patients, respectively. Other parameters accounted for an additional 6-10%. With respect to the relation between FER(HDL) and HDL subfractions, FER(HDL) related only to HDL2-C (males: r = -0.640, females: r = -0.652, P < 0.001). This result suggests that FER(HDL) is better able to predict the presence (or absence) of large HDL, rather than that of small HDL. All these data taken together, suggest that FER(HDL) is a useful tool to predict the particle size of both LDL and HDL, even in CHD patients.
OBJECTIVE: Lay-open pulmonary arterioplasty, a novel surgical technique to enlarge postoperative stenosis at the hilar pulmonary artery, was evaluated. METHODS: Lay-open arterioplasty, in which the enlarged hilar stenotic pulmonary artery is partially made up of previous surgical scar tissue instead of being covered by a patch, was performed on 10 patients whose ages ranged from 2.2 to 15.7 years. Surgical results were assessed by angiography. RESULTS: All patients tolerated the procedure without bleeding or embolic complications associated with pulmonary arterioplasty. Nine patients underwent concomitant procedures including total repair (n = 5), central interposing shunt (n = 3), and right ventricular outflow tract reconstruction (n = 1). No deaths or life-threatening events occurred during the total follow-up period of 18 patient-years. The stenotic segment was significantly enlarged from the preoperative diameter of 0.9 +/- 1.1 mm (mean +/- standard deviation) to the postoperative diameter of 8.0 +/- 1.3 mm, values which correspond to 7.0% +/- 8.8% and 68.4% +/- 11.5% of the normative values, respectively. A follow-up angiogram (n = 5) revealed an increase in the pulmonary artery diameter balanced with somatic growth (initial value, 65.2% +/- 9.0% of normal; second value, 69.1% +/- 7.7% of normal). No aneurysms or clinically significant restenoses were seen on the angiograms. CONCLUSIONS: Our initial midterm results with this method were promising. The pulmonary arteries subjected to this procedure grew in proportion to somatic growth.
Advanced glycation endproduct (AGE), whose formation is accelerated on long lived extracellular matrix proteins in diabetes, is implicated in diabetic complications in various tissues. Type I collagen is the predominant matrix protein of bone and plays an important role in bone cell-matrix interactions. We have previously reported the accelerated accumulation of AGE collagen in bone tissue in diabetes mellitus (DM), in which reduced bone mineral density was observed. In addition, when cultures of mature primary rat osteoblasts were plated onto an in vitro AGE-modified collagen substrate, they showed altered cell functions, in terms of alkaline phosphatase (ALP) activity, osteocalcin secretion, and nodule formation (J Bone Miner Res 11:931-937; 1996). To determine whether AGE collagen might also affect differentiation of preosteoblasts, we compared the effects of plating the preosteoblastic UMR 201-10B cell line onto AGE-modified collagen with plating onto unmodified collagen. The latter had been shown previously to promote differentiation of UMR 201 cells. We have also explored whether these effects might be partly mediated by the transforming growth factor beta (TGF-beta) receptor. Growth of UMR 201-10B cells on a type I collagen substrate significantly inhibited cell growth and retinoic acid (RA)-induced upregulation of ALP activity, compared to cells on plastic. These inhibitory effects were reduced by prior glycation of collagen, in a dose-dependent manner with respect to AGE content. Unmodified collagen stimulated production of osteopontin mRNA, which was reduced by AGE modification to levels attained in cells on plastic. Growth on control collagen inhibited TGF-beta type II receptor binding in 10B cells, while this inhibition was reduced by AGE modification. These data suggest that glycation of collagen interferes with specific interaction(s) between UMR 201-10B cells and collagen. Based on our previous results in UMR 201 cells, these results would be compatible with the notion that glycated collagen has reduced ability to promote differentiation of preosteoblasts to mature osteoblasts. These data further suggest that collagen-mediated events in these cells may be at least in part mediated by regulation of the TGF-beta receptor expression.
We report on a child who sustained blunt abdominal trauma with pancreatic duct rupture diagnosed by preoperative endoscopic retrograde pancreatography (ERP). Duct laceration remained undiagnosed by computerized tomography or ultrasonography. Preoperative ERP is the only known method for the accurate diagnosis of injury to main pancreatic duct. Even in children with pancreatic trauma we recommend ERP before any surgery is attempted to help in decisions on operative strategy.