Postoperative transient reduced diffusion in the ipsilateral striatum and thalamus.

BACKGROUND AND PURPOSE: Restriction of diffusion has been reported in the early phase of secondary neuronal degeneration, such as wallerian degeneration. The purpose of this study was to investigate postoperative transient reduced diffusion in the ipsilateral striatum and thalamus as a remote effect of surgery. MATERIALS AND METHODS: Six hundred two postoperative MR imaging examinations in 125 patients after cerebral surgery were retrospectively reviewed, focusing on the presence of reduced diffusion in the striatum and/or thalamus. The distribution of reduced diffusion in the striatum was classified into 3 groups: anterior, central, and posterior. Reduced diffusion in the thalamus was also classified on the basis of the anatomic locations of the thalamic nuclei. Further follow-up MRI was available in all patients with postoperative reduced diffusion, and acute infarctions were excluded. The patient medical records were reviewed to evaluate neurologic status. RESULTS: Restriction of diffusion was observed in the striatum and/or thalamus ipsilateral to the surgical site in 17 patients (13.6%). The distribution of signal abnormality correlated with the location of the operation, in concordance with the architecture of the striatocortical and thalamocortical connections. Reduced diffusion was observed from days 7 to 46 after the operation, especially during days 8-21. The signal abnormalities completely resolved on follow-up examinations. The median follow-up period was 202 days (interquartile range, 76-487 days). CONCLUSIONS: Postoperative transient reduced diffusion in the ipsilateral striatum and/or thalamus likely represents an early phase of secondary neuronal degeneration based on its characteristic distribution and time course. Clinically, this reduced diffusion should not be mistaken for postoperative ischemic injury.

Sarcoplasmic reticulum Ca2+ release is not a dominating factor in sinoatrial node pacemaker activity.

Recent work on isolated sinoatrial node cells from rabbit has suggested that sarcoplasmic reticulum Ca2+ release plays a dominant role in the pacemaker potential, and ryanodine at a high concentration (30 micromol/L blocks sarcoplasmic reticulum Ca2+ release) abolishes pacemaking and at a lower concentration abolishes the chronotropic effect of beta-adrenergic stimulation. The aim of the present study was to test this hypothesis in the intact sinoatrial node of the rabbit. Spontaneous activity and the pattern of activation were recorded using a grid of 120 pairs of extracellular electrodes. Ryanodine 30 micromol/L did not abolish spontaneous activity or shift the position of the leading pacemaker site, although it slowed the spontaneous rate by 18.9+/-2.5% (n=6). After ryanodine treatment, beta-adrenergic stimulation still resulted in a substantial chronotropic effect (0.3 micromol/L isoproterenol increased spontaneous rate by 52.6+/-10.5%, n=5). In isolated sinoatrial node cells from rabbit, 30 micromol/L ryanodine slowed spontaneous rate by 21.5+/-2.6% (n=13). It is concluded that sarcoplasmic reticulum Ca2+ release does not play a dominating role in pacemaking in the sinoatrial node. The full text of this article is available at http://www.circresaha.org.

Studies on the constituents of bark of Parameria laevigata Moldenke.

One new trimeric proanthocyanidin, epicatechin-(2beta-->O-->7, 4beta-->6)-epicatechin-(2beta-->O--->7, 4beta-->8)-epicatechin (5) and two new tetrameric proanthocyanidins, epicatechin-(2beta-->O-->7, 4beta-->8)-[epicatechin-(4beta-->6)]-epicatechin-(4beta-->8)-epicatechin, named as parameritannin A-1 (6), and epicatechin-(2beta-->O-->5, 4beta-->6)-[epicatechin-(2beta-->O-->7, 4beta-->8)]-epicatechin-(4beta-->8)-epicatechin, named as parameritannin A-2 (7), have been isolated from the bark of Parameria laevigata Moldenke (Apocynaceae) along with the two known dimers, proanthocyanidin A-2 (1) and proanthocyanidin A-6 (2), and two trimers, cinnamtannin B-1 (3) and aesculitannin B (4). These structures were elucidated by spectral and chemical evidence.

Murine and human SDF2L1 is an endoplasmic reticulum stress-inducible gene and encodes a new member of the Pmt/rt protein family.

We isolated murine and human cDNAs for SDF2L1 (stromal cell-derived factor 2-like1) and characterized the genomic structures. Northern blot analysis of the gene expression in various tissues revealed that both murine Sdf2l1 and human SDF2L1 genes are expressed ubiquitously, with particularly high expression in the testis. The SDF2L1 protein has an endoplasmic reticulum (ER)-retention-like motif, HDEL, at the carboxy (C)-terminus. Interestingly, SDF2L1 protein also shows significant similarity to the central hydrophilic part of protein O-mannosyltransferase (Pmt) proteins of Saccharomyces cerevisiae, the human homologues of Pmt (POMT1 and POMT2) and Drosophila melanogaster rotated abdomen (rt) protein. In a murine hepatocellular carcinoma cell line, Sdf2l1 was strongly induced by tunicamycin and a calcium ionophore, A23187, and weakly induced by heat stress but was not induced by cycloheximide. In conclusion, SDF2L1 protein is a new member of Pmt/rt protein family and Sdf2l1 is a new ER stress-inducible gene.

The cytoprotective role of lipopolysaccharide-induced nitric oxide against liver damage during early phase of endotoxemia in rats.

Lipopolysaccharide (LPS)-induced endotoxemia produces nitric oxide (NO); however, the role of the NO during endotoxemia is still controversial. The aim of this study was to investigate a role of LPS-induced NO during the early phase of endotoxemia. Wistar rats were intraperitoneally injected with saline or LPS at various doses (0.001, 0.01, or 5 mg/kg), and intra-abdominal NO concentration was determined by chemiluminescence before and after LPS administration at indicated times (1, 2, 6, 10, and 18 h). Serum aspartate aminotransferase and alanine aminotransferase levels were determined and histological examination was performed 10 h after LPS administration to assess liver damage. N(G)-nitro-L-arginine-methyl ester (L-NAME), a nonselective inhibitor of NO synthase, was used to investigate the possible roles of NO during LPS-induced endotoxemia. The intra-abdominal NO concentration was elevated within 2 h and reached a maximal level at 10 h after low doses of LPS injection (0.001 and 0.01 mg/kg) while liver damage was not observed. After high-dose LPS (5 mg/kg) administration, liver damage was observed and intra-abdominal NO was elevated continuously until 18 h. A time course study revealed very similar patterns of intra-abdominal NO increase after the three different dose of LPS at each times points during the first 10 h. Pretreatment of L-NAME inhibited the intra-abdominal NO release and aggravated the liver damage caused by low doses (0.001 and 0.01 mg/kg) of LPS as well as high dose (5 mg/kg) of LPS. Therefore, NO, released during the first 10 h after LPS injection, may play a cytoprotective role in the liver.

Vesnarinone prolongs action potential duration without reverse frequency dependence in rabbit ventricular muscle by blocking the delayed rectifier K+ current.

BACKGROUND: Methanesulfonanilide derivatives, selective inhibitors of the rapidly activating component (I(Kr)) of the delayed rectifier potassium current (I(K)), prolong action potential duration (APD) of cardiac muscles with reverse frequency dependence, which limits their clinical use because of proarrhythmia. Vesnarinone, a quinolinone derivative developed as a cardiotonic agent, has complex pharmacological properties, but its clinical efficacy is explained in part by I(K) reduction. Therefore, we investigated the mode of I(K) block by vesnarinone. METHODS AND RESULTS: I(K) of the rabbit ventricular myocyte was activated by voltage-clamp steps applied from a holding potential to various depolarizing levels. The development of I(K) block at depolarization (+10 mV) and its recovery process at hyperpolarization (-75 mV) were compared between vesnarinone and E-4031. The I(K) block by vesnarinone (3 micromol/L) developed and recovered monoexponentially, with time constants of 361 ms (n=5) and 1.87 seconds (n=4), respectively. I(K) block by E-4031 (0.3 micromol/L) developed instantaneously, with no recovery from the block at hyperpolarization. The I(K) block by vesnarinone, estimated by I(K) tail after a train of depolarizing pulses (for 30 seconds at 0.2 to 2 Hz), was increased with increasing frequency (twofold at 2 from 0.2 Hz), but that by E-4031 was unchanged. In rabbit papillary muscles, vesnarinone (10 micromol/L) prolonged APD at stimulation frequencies >0.2 Hz, whereas E-4031 (0.3 micromol/L) prolonged that in a reverse frequency-dependent manner. CONCLUSIONS: Vesnarinone may prolong the repolarization of human cardiac muscle without reverse frequency dependence, because I(Kr) is expressed in humans as well as in the rabbit. Thus, this drug may be a model for an ideal class III drug without the risk of proarrhythmia.

Evidences of antagonism between amiodarone and triiodothyronine on the K+ channel activities of cultured rat cardiomyocytes.

Effects of acute and chronic treatments with amiodarone, both in the presence and the absence of exogenous triiodothyronine (T3), on repolarizing outward K+ currents were investigated by patch-clamp technique in cultured newborn rat ventricular cells. Acute exposure to amiodarone dose-dependently inhibited the transient outward (Ito IC50 = 4.9 microM) and the steady-state outward (IK, IC50 = 6.3 microM) K4 currents. The dose-response curve of this acute inhibitory action was unaffected by the presence of T3. When amiodarone was applied chronically. 72-h exposure to a low dose of the drug (1 microM) significantly decreased the current densities of Ito and I kappa for the cells cultured in a serum-supplemented medium containing 0.12 nM T3. In a serum-free medium without T3o chronic amiodarone treatment revealed null effect on either Ito or IK. In addition, 72-h in-vitro treatment with Ti enhanced the current densities of both Ito (EC50 = 0.13 nM) and I kappa (EC50 = 0.33 nM). Concentration-response analysis indicated that amiodarone (1 microM) showed competitive inhibition towards the action of T3 on Ito but noncompetitive inhibition towards the action of T3 on IK. These results suggest that different ionic mechanisms are produced by acute and long-term treatments with amiodarone. The latter showed T3-dependent inhibition of cardiac Ito and IK. When chronically administered, amiodarone may antagonize T3 and thereby counteract its hormonal effect on K+ channels. This implies that, at the myocyte level, antagonism of the action of thyroid hormones in K+ channel activities may contribute to the cardiac effects of chronic amiodarone therapy.

[Exposure to blood during midwifery operations--a questionnaire study].

A self-administered questionnaire was mailed to all midwives working in Nara Prefecture to investigate blood exposure events at delivery and to consider protective measures for the exposure. Out of the 203 midwives 193 responded to the questionnaire. The median number of deliveries in which the midwives had assisted within the past one year was 35 after excluding those who had not assisted in deliveries at all. The incidence of needle-stick injuries was estimated to be 86.2 per 100 persons within the past one year. The occurrence in the subgroup who had worked as midwife for less than 5 years was 2-3 times higher than that in those who worked for more than 5 years. Over 90% of the midwives had experiences of direct blood contact events to the skin while assisting in their 10 most recent deliveries. Blood contact events occurred in the finger-hand-arm area in 85% of the midwives, on the legs in 62%, in the face in 20% and in the eyes in 1%. Around 20% of the midwives had unintentionally sucked amniotic fluid when using a tracheal catheter on a newborn. The most common occasion where direct blood contact events occurred was while bathing an infant for removing blood and amniotic fluid. The midwives wore a disposal gown more often when assisting in labors of parturient women infected with blood-born infectious diseases than without the diseases, and similarly for wearing gloves when measuring blood loss and for usage of a mechanical device for sucking amniotic fluid in the tracheae of an infant. Based on the results obtained in this questionnaire study and our previous study about blood contact events observed in a delivery room, protective measures for midwives against exposure to blood at delivery are required and some ideas are presented.

[Exposure to blood during midwifery procedures--blood contact events to midwives occurred in a delivery room].

Midwives are often exposed to blood during delivery procedures. A study aimed at clarifying actual status of blood contact during midwifery procedures was performed. Observations in a delivery room were conducted to record blood contact events experienced by midwives from the time of episiotomy until 2 hour after expulsion of the placenta. All gloves used by midwives were collected and tested for holes. Blood contact was defined as any contact with blood of a parturition woman as recognized visually by an observer. During a one-month study period data was obtained from a total of 19 midwives (12 midwives and 7 student midwives) who assisted in 8 deliveries. All of the midwives wore gowns with long sleeves, gloves and caps but did not use eye protection or masks. None of the parturient women had Hepatitis B, Hepatitis C or acquired immunodeficiency syndrome. Deliveries caused widespread blood exposure to the midwives throughout the complete course. Protection from most of this exposure was provided by the gowns and gloves. However, direct blood contacts occurred to the fingers, hands or forearms in several midwives. These events were caused by partly because the midwives unintentionally performed procedures without gloves and partly because blood penetrated the gown and soaked to the skin. Direct blood contacts to the foot in two midwives and to the mouth in one also occurred. The overall perforation rate for gloves examined was 4 out of 154 (2.6%). Two gloves were broken during washing sharp instruments contaminated with blood, one was torn when wearing, and the remaining one appeared to have had a hole prior to use.(ABSTRACT TRUNCATED AT 250 WORDS)

Investigation of normal pressure hydrocephalus by 123I-IMP SPECT.

We evaluated N-isopropyl-p-[123I]iodoamphetamine (123I-IMP) single photon emission computed tomography (SPECT) as a method for identifying normal pressure hydrocephalic (NPH) patients eligible for shunting procedures. 123I-IMP SPECT scans were taken before and after cerebrospinal fluid (CSF) taps in NPH cases. Post-subarachnoid hemorrhagic (SAH) patients showed apparent frontal blood flow reduction but non-SAH cases did not. The frontal blood flow increased in comparison with the temporal flow after CSF tapping in SAH cases who benefited most from shunting. Cerebral blood flow study before and after CSF removal is a potential method for classifying NPH patients likely to benefit from the shunting operation.

Induction of transplantable tumors by repeated subcutaneous injections of natural and synthetic vitamin E in mice and rats.

Natural vitamin E and synthetic vitamin E (dl-alpha-tocopheryl acetate) were tested for their tumorigenicity in rodents. Transplantable tumors, at the site of injection, were induced by repeated injections of these compounds in two strains of mice, NFS/N and C57BL/6N x C3H/He F1, and in a strain of rats, Fischer 344. Natural vitamin E was tumorigenic in both strains of female mice only when injected with soya oil. In contrast, dl-alpha-tocopheryl acetate alone was capable of inducing tumors in Fischer 344 rats. Only one out of 5 male NFS/N mice given dl-alpha-tocopheryl acetate developed a tumor. Therefore, Fischer 344 rats were more susceptible to tumor formation by dl-alpha-tocopheryl acetate than NFS/N mice. dl-alpha-Tocopheryl acetate with soya oil or with palm oil also resulted in the formation of transplantable tumors in NFS/N mice and Fischer 344 rats. There was no difference in the tumor incidence between mice treated with dl-alpha-tocopheryl acetate alone and dl-alpha-tocopheryl acetate plus soya oil or palm oil. However, in rats, the incidence was lower for a group treated with dl-alpha-tocopheryl acetate plus palm oil than for those with dl-alpha-tocopheryl acetate alone and with dl-alpha-tocopheryl acetate plus soya oil.

[A carcinoma of the cecum arising from the orifice of the appendix: a case report].

Reported is the case of a 50-year-old man who was admitted to hospital because of an abdominal pain. A barium enema revealed the shade of a distended, unfilled appendix that had reversed itself on the cecum and the ascending colon, the latter showing compression from the exterior. Further, a colonoscopic examination uncovered a flat, nodular tumor of the cecum that had elevated at the orifice of the vermiform appendix, and 67Ga scintigraphy indicated the uptake at the lower right abdomen. A resected specimen of the tumor showed proliferation in the cecal mucosa at the orifice of the appendix, causing an appendiceal abscess, and the histopathological findings revealed an adenocarcinoma of the cecal mucosa but no malignant transformation of the appendiceal mucosa.

[Effect of diltiazem on experimental cerebral vasospasm incomparison with effects of cinnarizine, verapamil and nifedipine].

The contractile activity of arterial muscle cells is controlled by the intercellular free Ca2+ concentration. The membrane systems of both the cell surface and internal organs, seem to be responsible for controlling the myoplasmic Ca2+ level. The mechanism of action of Ca2+ antagonists, typified by verapamil and nifedipine, has been postulated to be a blockade of transmembrane calcium influx. In this study, the vasodilating effect of diltiazem on experimental cerebral vasospasm in vivo was examined using dogs and was compared with those of cinnarizine, verapamil and nifedipine which have already been reported by us. Cerebral vasospasms were induced in adult dogs by injecting 5 ml of fresh arterial blood into the cisterna magna. 10(-6)M diltiazem was injected by one shot into the vertebral artery with cerebral vasospasm. Dilatation of the cerebral arteries were monitored by angiography after administration of diltiazem. Blood pressure, intracranial pressure and pulse rate were measured during intravenous application of the drug in normal animals. Administration of diltiazem released the vasospasm for 30 minutes comparable to the times of the other Ca2+ antagonists. Diltiazem had cerebral vasodilator actions similar to cinnarizine at doses that did not decrease systemic blood pressure, while the other drugs decreased intracranial pressure slightly and nifedipine decreased pulse rate slightly. Therefore, we consider diltiazem to be satisfactory for the treatment of experimental cerebral vasospasm.