Biomedical subjects

Y Kikuchi

Publications and source records attributed to Y Kikuchi.

At least 307 records · Page 17Linked to original sources

PubMed1996

Demonstration of a cross-talk between IL-2 and IL-5 in phosphorylation of IL-2 and IL-5 receptor beta chains.

We have examined phosphorylation mediated by cross-talk between growth signal pathways induced by IL-2 and IL-5. To analyze the phosphorylation process in the same cells, we established two sublines, T88-Mbeta1, which is a subline of a murine IL-5-dependent cell line, T88-M, by introduction of the human IL-2 receptor beta chain (IL-2Rbeta), and secondly CTLL-5Ralphabeta, which is a subline of a murine IL-2-dependent cell line, CTLL-2, by introduction of the murine IL-5 receptor alpha chain (IL-5Ralpha) and IL-5 receptor beta chain (IL-5Rbeta, betac) genes. Both T88-Mbeta1 and CTLL-5Ralphabeta expressed high-affinity receptors for IL-2 and IL-5, and proliferated in response to both factors. Tyrosine phosphorylation of IL-2Rbeta was induced by stimulation of T88-Mbeta1 with not only IL-2 but also IL-5. Anti-IL-2Rbeta-directed immune complexes from T88-Mbeta1 stimulated with IL-5 as well as with IL-2 contained an activated tyrosine kinase. However, stimulation with IL-5 but not IL-2 induced the tyrosine phosphorylation of IL-5Rbeta, betac, suggesting that IL-2 does not activate a tyrosine kinase which efficiently catalyzes the IL-5Rbeta molecule in response to IL-5. On the other hand, the detection of JAK1 and the other common set of phosphotyrosine-containing proteins after stimulation with either IL-5 or IL-2 suggests the existence of the same tyrosine phosphorylation pathways.

Animals↗

PubMed1996

Purification and characterization of the DNA-binding domain of BTEB, a GC box-binding transcription factor, expressed in Escherichia coli.

BTEB is a GC-binding protein that regulates the transcription of genes with a single GC-box or tandemly repeated GC-boxes in the promoter. The DNA-binding domain of BTEB consists of three contiguous Cys2-His2 zinc finger motifs and short segments adjacent to their N- and C-terminal sides [Kobayashi et al. (1995) J. Biochem. 117, 91-95]. The truncated BTEB (residues 120 to 244) containing the DNA-binding domain was expressed in Escherichia coli and purified to homogeneity under denaturing conditions. DNA-binding activity of the BTEB was regenerated by refolding in the presence of Zn2+. The efficiency in regeneration was 70 +/- 10%, and the dissociation constant (Kd) of the DNA-complex was 4 +/- 2 nM. Co2+ also regenerated the DNA-binding affinity of BTEB, albeit with less efficiency than Zn2+. Co-BTEB showed a slightly lower affinity to the specific DNA than Zn-BTEB. Refolding in the presence of Cd2+ resulted in an extremely low efficiency in regeneration of the DNA-binding activity. Zn-BTEB is in a monomer state at concentrations lower than 0.5 microM, and forms a dimer in the concentration range of about 10 to 200 microM.

Amino Acid Sequence↗

PubMed1996

The role of nitric oxide in mouse cerulein-induced pancreatitis with and without lipopolysaccharide pretreatment.

Nitric oxide (NO) has been shown to play a significant role in inflammation. To clarify the role of NO in acute pancreatitis, we investigated the serum concentrations of NO chi (NO2- plus NO3-) and tumor necrosis factor-alpha (TNF-alpha) and the grade of pancreatitis in cerulein-induced pancreatitis in mice pretreated with lipopolysaccharide (LPS) or not. LPS pretreatment aggravated the cerulein pancreatitis in association with a transient increase in serum TNF-alpha, which was followed by a gradual elevation of serum NO chi. This elevation of serum NO chi concentration was inhibited by the NO synthase inhibitor NG-nitro-L-arginine (L-NNA). In addition, the activity of NADPH-diaphorase (NADPH-d), a marker for NO synthase, appeared in the peritoneal macrophages of LPS-pretreated mice after the induction of pancreatitis. No elevation of serum NO chi or appearance of NADPH-d activity in peritoneal cells was found in mice without LPS pretreatment. Administration of L-NNA enhanced the elevation of pancreatitis-induced serum amylase in mice untreated with LPS, while L-NNA inhibited the elevation in LPS-pretreated mice. The effects of L-NNA were reversed by the administration of L-arginine but were not affected by D-arginine. These results suggested that (a) inflammatory cells may not be fully activated to produce excessive NO in uncomplicated edematous pancreatitis, and (b) edematous pancreatitis may be aggravated by excessively produced NO if bacterial infection is complicated and inflammatory cells are activated to express inducible NO synthase.

Animals↗

PubMed1996

The role of pituitary-adrenal counterregulation of inflammation in cerulein-induced pancreatitis: a comparison between Fischer and Lewis rats.

The role of the hypothalamic-pituitary-adrenal axis (HPA axis) in acute pancreatitis has not yet been clarified. In the present study, the concentrations of serum corticosterone and amylase, the severity of pancreatic edema, and the histology of the pancreas during cerulein-induced pancreatitis were compared in two strains of rats whose HPA axes have been reported to be hyperresponsive (Fischer female) and hyporesponsive (Lewis female) to inflammatory mediators. First, we confirmed that the secretory response of corticosterone to lipopolysaccharide was remarkably blunted in Lewis rats compared with Fischer rats. With a single intraperitoneal injection of cerulein at a dose of 50 micrograms/kg, the serum corticosterone of Fischer rats increased promptly, and their serum levels were significantly higher than those of Lewis rats at all points after the induction of pancreatitis. The edema formation and infiltration of inflammatory cells into the pancreas were more severe in Lewis rats than in Fischer rats. The serum amylase concentration was not significantly different between the two strains, except at 2 h after the induction of pancreatitis. The in vitro study using dispersed pancreatic acini showed that there was no significant difference in cerulein-stimulated amylase secretion between the two strains. These findings suggest that the responsiveness of the HPA axis and the consequent secretion of glucocorticoids might modify the pathological features of acute pancreatitis.

Acute Disease↗

PubMed1996

Insertion of a pacing lead via the tricuspid valve does not affect cardiac function and tricuspid valve regurgitation in young dogs.

A preliminary experimental study in dogs was conducted to evaluate the feasibility of transvenous cardiac pacing in the fetus with complete heart block associated with hydrops. Four young mongrel dogs were anesthetized with intravenous administration of sodium pentobarbital and mechanically ventilated, and a pacing lead was inserted via the tricuspid valve. The right ventricular cardiac output, aortic pressure and central venous pressure were measured, and the tricuspid valve regurgitation was measured semi-quantitatively using echo-Doppler color flow imaging. The relationship between the location of the pacing lead and the tricuspid valve regurgitation and cardiac function was examined. The mean right ventricular cardiac output when the pacing lead was inserted into the superior vena cava (126 +/- 54 mL/min per kg) was not significantly different from that when it was inserted into the right ventricle (110 +/- 43 mL/min per kg). The aortic pressure was 66 +/- 7.7 mmHg and 67 +/- 6.6 mmHg, respectively, and the central venous pressure 5.9 +/- 1.7 mmHg and 5.7 +/- 1.6 mmHg, respectively, under the two conditions (not significantly different). The ratio of demonstrating significant tricuspid valve regurgitation was 4/13 into the superior vena cava and 5/13 into the right ventricle, respectively (not significantly different). The location of the pacing lead did not change the cardiac function or the amount of the tricuspid valve regurgitation in our experimental study. It was therefore concluded that the transvenous cardiac pacing technique has potential application in intrauterine transvenous cardiac pacing in the fetus with complete heart block.

Age Factors↗

PubMed1996

Correlation between the stimulatory effect of oxytocin on the formation of inositol phosphates and the oxytocin receptor level in the pregnant rabbit myometrium.

OBJECTIVE: In order to elucidate the roles of inositol trisphosphate (IP3) and oxytocin (OT) receptors in rabbit parturition, the concentration of IP3 induced by OT and the OT receptor levels were determined in rabbit myometria before and after parturition. METHODS: The effects of OT on IP3 formation and OT receptor levels were determined in the myometria of non-pregnant rabbits, Days 26, 28 and 30 of pregnancy rabbits, postpartum rabbits within 12 hours and steroid-treated ovariectomized rabbits. Prostaglandins (PGs) levels were also measured in the myometrial and decidual tissues. RESULTS: OT receptors were not detectable in the myometria of non-pregnant rabbits, and OT had no effect on the formation of inositol phosphates (IPs). On Day 28 of pregnancy, OT receptors became detectable, and then OT could induce the formation of IPs. Thereafter, the stimulatory effects of OT on IPs formation and the OT receptor levels dramatically increased toward the end of pregnancy and reduced rapidly after parturition. When the ovariectomized pregnant rabbits were treated with estrogen, OT receptors in the myometrium were induced, and OT acquired the ability to stimulate IP3 formation. However, OT had no effect on the production of cAMP, cGMP, prostaglandin (PG) E2 and F2 alpha in the myometria, even if receptors existed, although PGE2 production in the decidual tissues was markedly stimulated. In addition, an OT receptor antagonist inhibited the stimulatory effects of OT on IP3 formation. CONCLUSIONS: These results suggest that the formation of IPs by OT, the OT receptor levels in the myometrium, and the production of PGF2 in the decidua might play crucial roles in parturition.

Animals↗

PubMed1996

Two new members of the murine Sim gene family are transcriptional repressors and show different expression patterns during mouse embryogenesis.

From a cDNA library of mouse skeletal muscle, we have isolated mouse Sim1 (mSim1) cDNA encoding a polypeptide of 765 amino acids with striking amino acid identify in basic helix-loop-helix (89% identify) and PAS (89 % identify) domains to previously identified mSim2, although the carboxy-terminal third of the molecule did not show any similarity to mSim2 or Drosophila Sim (dSim). Yeast two-hybrid analysis and coimmunoprecipitation experiments demonstrated that both of the mSim gene products interacted with Arnt even more efficiently than AhR, a natural partner of Arnt, suggesting a functional cooperativity with Arnt. In sharp contrast with dSim having transcriptional-enhancing activity in the carboxy-terminal region, the two mSims possessed a repressive activity toward Arnt in the heterodimer complex. This is the first example of bHLH-PAS proteins with transrepressor activity, although some genetic data suggest that dSim plays a repressive role in gene expression (Z. Chang, D. Price, S. Bockheim, M. J. Boedigheimer, R. Smith, and A. Laughon, Dev. Biol. 160:315-322, 1993; D. M. Mellerick and M. Nirenberg, Dev. Biol. 171:306-316, 1995). Whole-mount in situ hybridization showed restricted and characteristic expression patterns of the two mSim mRNAs in various tissues and organs during embryogenesis, such as those for the somite, the nephrogenic cord, and the mesencephalon (for mSim1) and those for the diencephalon, branchial arches, and limbs (for mSim2). From sequence similarity and chromosomal localization, it is concluded that mSim2 is an ortholog of hSim2, which is proposed to be a candidate gene responsible for Down's syndrome. The sites of mSim2 expression showed an overlap with the affected regions of the syndrome, further strengthening involvement of mSim2 in Down's syndrome.

Amino Acid Sequence↗

PubMed1996

Bul1, a new protein that binds to the Rsp5 ubiquitin ligase in Saccharomyces cerevisiae.

We characterized a temperature-sensitive mutant of Saccharomyces cerevisiae in which a mini-chromosome was unstable at a high temperature and cloned a new gene which encodes a basic and hydrophilic protein (110 kDa). The disruption of this gene caused the same temperature-sensitive growth as the original mutation. By using the two-hybrid system, we further isolated RSP5 (reverses Spt- phenotype), which encodes a hect (homologous to E6-AP C terminus) domain, as a gene encoding a ubiquitin ligase. Thus, we named our gene BUL1 (for a protein that binds to the ubiquitin ligase). BUL1 seems to be involved in the ubiquitination pathway, since a high dose of UBI1, encoding a ubiquitin, partially suppressed the temperature sensitivity of the bul1 disruptant as well as that of a rsp5 mutant. Coexpression of RSP5 and BUL1 on a multicopy plasmid was toxic for mitotic growth of the wild-type cells. Pulse-chase experiments revealed that Bul1 in the wild-type cells remained stable, while the bands of Bul1 in the rsp5 cells were hardly detected. Since the steady-state levels of the protein were the same in the two strains as determined by immunoblotting analysis, Bul1 might be easily degraded during immunoprecipitation in the absence of intact Rsp5. Furthermore, both Bul1 and Rsp5 appeared to be associated with large complexes which were separated through a sucrose gradient centrifugation, and Rsp5 was coimmunoprecipitated with Bul1. We discuss the possibility that Bul1 functions together with Rsp5 in protein ubiquitination.

Adaptor Proteins, Signal Transducing↗

PubMed1996

"Cross talk" between the bioactive glycerolipids and sphingolipids in signal transduction.

Hydrolysis of phosphatidylcholine via receptor-mediated stimulation of phospholipase D produces phosphatidate that can be converted to lysophosphatidate and diacylglycerol. Diacylglycerol is an activator of protein kinase C, whereas phosphatidate and lysophosphatidate stimulate tyrosine kinases and activate the Ras-Raf-mitogen-activated protein kinase pathway. These three lipids can stimulate cell division. Conversely, activation of sphingomyelinase by agonists (e.g., tumor necrosis factor-alpha) causes ceramide production that inhibits cell division and produces apoptosis. If ceramides are metabolized to sphingosine and sphingosine 1-phosphate, then these lipids can stimulate phospholipase D and are also mitogenic. By contrast, ceramides inhibit the activation of phospholipase D by decreasing its interaction with the G-proteins, ARF and Rho, which are necessary for its activation. In whole cells, ceramides also stimulate the degradation of phosphatidate, lysophosphatidate, ceramide 1-phosphate, and sphingosine 1-phosphate through a multifunctional phosphohydrolase (the Mg(2+)-independent phosphatidate phosphohydrolase), whereas sphingosine inhibits phosphatidate phosphohydrolase. Tumor necrosis factor-alpha causes insulin resistance, which may be partly explained by ceramide production. Cell-permeable ceramides decrease insulin-stimulated glucose uptake in 3T3-L1 adipocytes after 2-24 h, whereas they stimulate basal glucose uptake. These effects do not depend on decreased tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 or the interaction of insulin receptor substrate-1 with phosphatidylinositol 3-kinase. They appear to rely on the differential effects of ceramides on the translocation of GLUT1-and GLUT4-containing vesicles. It is concluded that there is a significant interaction and "cross-talk" between the sphingolipid and glycerolipid pathways that modifies signal transduction to control vesicle movement, cell division, and cell death.

Animals↗

PubMed1996

Unilateral smoke inhalation in sheep: effect on left lung lymph flow with right lung injury.

We previously reported that smoke inhalation to the right lung will result in damage to the air-insufflated left lung. In this study we confirm these findings and determine whether this injury is associated with an elevation in lung lymph flow and pulmonary microvascular permeability to protein as indexed by changes in reflection coefficient. Sheep (n = 12) were surgically prepared by placement of a Swan-Ganz catheter and pneumatic occluders on all pulmonary veins and the left pulmonary artery. The left lung lymphatic was selectively cannulated as shown previously (Y. Kikuchi, H. Nakazawa, and D. Traber. Am. J. Physiol. 269 (Regulatory Integrative Comp. Physiol. 38): R943-R947, 1995). All afferent lymphatics from the right lung were severed, and the right pulmonary ligament was sectioned. The caudal end of the lymph node was sectioned to remove systemic lymph contamination. The sheep were studied in the unanesthetized state 7 days later. To ensure that lymph flow was exclusively from the left lung (QLL), right pulmonary microvascular pressure was increased, a procedure that resulted in little or no change in QLL, as was previously shown. The sheep were then anesthetized, and a Carlens tube was positioned to allow separate ventilation of the right and left lung. The right lungs of five sheep and the left lungs of two sheep were insufflated with cotton smoke. Insufflation of the left lung with cotton smoke produced a fourfold increase in QLL that began 4 h after insult. Insufflation of the right lung with smoke led to a doubling of QLL that began 12 h after insult. Changes in QLL were associated with increased microvascular permeability, as indexed by the reflection coefficient. Control sheep (air insufflated into both lungs, n = 5) showed no change in QLL. Injury to the right lung resulted in damage to the left air-insufflated lung, suggesting a hematogenous mediation of the response.

Animals↗

PubMed1996

Leukopenia and rheological anomalies in leukocytes during hemodialysis in patients with chronic renal failure.

In order to clarify the relation between leukopenia during hemodialysis and leukocyte adhesiveness, the number of circulating leukocytes, their filterability through 5 micron diameter pores, and the concentration of neutrophil elastase in plasma were measured in peripheral blood collected at the beginning of hemodialysis (dialyzer, cuprophane membrane), 15 min into dialysis, and end of dialysis (duration of dialysis, 180 min) in 15 patients with chronic renal failure. Leukopenia was most marked at 15 min in all patients. In accordance with the change in number of circulating leukocytes, the filtration time of the leukocytes, as determined by a modification of the Nuclepore filtration method (filtered blood volume 0.5 ml, leukocyte count 2,500 microliters, suction pressure 10 cm H2O temperature 37 degrees C) was significantly longer at 15 min versus the beginning and end of the dialysis (p < 0.005 and p < 0.025, respectively). Addition of the chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP; 20 nM), to the suspensions immediately increased the leukocyte filtration time. Such FMLP-induced increases were significantly greater at 15 min versus the beginning of dialysis (p < 0.05). This heightened sensitivity of cells to FMLP appeared to persist until the end of dialysis (p < 0.05 versus the beginning). Plasma levels of neutrophil elastase were highest at the end of dialysis versus those at the beginning and after 15 min (both p < 0.005). Results suggest that the changes in filterability of leukocytes may be related to decreases in their number in the circulation. Neutrophil elastase appeared to accumulate in plasma so that its maximal value at the end of dialysis would reflect the preceding changes in leukocyte rheology.

Adult↗

PubMed1996

Effect of culture supernatants of endometriotic lesions, uterine endometrium and peritoneum from rats with experimental endometriosis on the natural killer activity of spleen cells.

Experimental endometriosis in rats was induced by autotransplanting the uterine endometrium to the peritoneum. In all rats, endometrial implants developed into endometriotic tissues similar to those in humans about 2 weeks after transplantation. Natural killer (NK) activity of spleen cells in the endometriosis model rats was significantly (p < 0.05) lower than that in the sham-operated intact rats. The inhibited NK activity in the endometriosis rats recovered to the level in intact rats with danazol (but not buserelin). The supernatant after 24-hour culture of endometrial tissues from both intact and model rats seemed to have significant inhibitory effects on NK activity. The supernatant from endometrial grafts showed significantly (p < 0.05) higher inhibitory effects than that from the endometrial tissues. The inhibitory effects were significantly (p < 0.05) reduced by treatment with danazol or buserelin to the untreated level. In addition, supernatants of unaffected peritoneal tissues from the endometriosis rats had significantly (p < 0.01) higher inhibitory effects on NK activity than those from the intact rats. Even when uterine serosa or silicone was implanted to the peritoneum, the supernatants of the contralateral peritoneal tissues showed significantly (p < 0.05) higher inhibitory effects than those from the intact rats, while having significantly (p < 0.05) lower inhibitory effects than those from the endometriosis rats. These results suggest that this marked inhibitory effect on NK activity by the peritoneum may be associated with the development and progression of endometriosis.

Animals↗

PubMed1996

N-acetylcysteine inhibits loss of diaphragm function in streptozotocin-treated rats.

We examined whether streptozotocin (STZ)-induced diabetic rats have an impairment in diaphragm contractility, and if so, whether N-acetylcysteine (NAC), a nonspecific antioxidant, prevents this impairment. First, diaphragm contractility, assessed by tension-frequency relationships and twitch kinetics in in vitro diaphragm strip preparations of Wistar rats, was obtained on Days 3 and 7 after administration of STZ of 30 or 60 mg/kg body weight, and compared with that of the control group. Second, NAC at 500 mg/kg body weight or vehicle solution was administered orally every day in rats treated with STZ at 60 mg/kg body weight, and diaphragm function on Day 7 after starting NAC treatment was compared between vehicle control and STZ-treated groups. We found that diaphragm function in STZ-treated rats, which had hyperglycemia, decreased in a dose- and time-dependent manner. NAC inhibited the decrease in diaphragm contractility in STZ-treated rats without reducing blood glucose. These findings suggest that the loss of diaphragm function in STZ-induced diabetic rats is not directly related to hyperglycemia. The data are consistent with secondary alterations of normal cytokine signaling or changes in the redox state of the cell, both of which could be affected by NAC treatment.

Acetylcysteine↗

PubMed1996

A novel calcium-binding protein in amniotic fluid, CAAF1: its molecular cloning and tissue distribution.

We found by using a 45Ca2+ overlay technique a large amount of Ca(2+)-binding activity in bovine amniotic fluid from which a novel calcium-binding protein (CaBP) was purified and is referred to as CAAF1 (calcium-binding protein in amniotic fluid-1), with an apparent molecular mass of 8 kDa determined by N-tris(hydroxymethyl)-methylglycine/ SDS-PAGE. It was structurally homologous with MRP/calgranulin proteins (MRP8/calgranulin A and MRP14/calgranulin B), members of the S100 protein family, which are abundantly found in the cytoplasm of granulocytes and macrophages. CAAF1 lacked the predicted signal peptide sequence, which is consistent with other CaBPs. The tissue and cellular distribution of CAAF1 was determined by monoclonal antibodies developed against this protein. Its immunoreactivity was found in squamous epithelial cells, neutrophils, and some macrophages throughout the fetal body. An especially characteristic staining pattern was obtained in the squamous epithelium, including that of the esophagus, skin and amnion: CAAF1 was detected in the suprabasal squamous epithelial cells undergoing differentiation, but not in the cells in the proliferating basal layer. Northern blot analysis also showed that CAAF1 mRNA was highly expressed in bovine fetal esophagus and skin. On the other hand, our ELISA studies showed that CAAF1 protein was present in amniotic fluid at a concentration of about 120 nM, which was over 30 times as high as that in the fetal serum. These results suggested that CAAF1 is one of the stage-specific proteins in the differentiation of squamous epithelial cells, and that CAAF1 is preferentially produced by fetal squamous epithelial cells, including epidermal keratinocytes and amniotic epithelial cells, and it is stored in the amniotic fluid during embryogenesis.

Amino Acid Sequence↗

PubMed1996

The culture fluid of Isaira japonica yasuda augments anti-sheep red blood cell antibody response in mice.

Isaria japonica YASUDA was cultured in a liquid medium, and its culture fluid (IJCE) was tested for stimulatory activity to humoral antibody production. IJCE significantly enhanced the production of anti-sheep red blood cell (SRBC) plaque forming cells (PFC) by oral ingestions at 10 and 30 mg/kg/d for 4 consecutive days, either before or after SRBC challenge. It also recovered the reduction of anti-SRBC PFC response and number of spleen cells caused by treatment with 5-fluorouracil. It is suggested that IJCE is a promising source for an immunomodulating tool or medicine.

Adjuvants, Immunologic↗

PubMed1996

Is the intracellular pH threshold an anaerobic threshold from the view point of intracellular events?: a brief review.

Intracellular biochemical changes could be monitored noninvasivery and continuously by using nuclear magnetic resonance (NMR). In about the last decade, intracellular behavior of phosphorus compounds and pH during muscle contraction in man have been studied by 31P nuclear magnetic resonance spectroscopy (31P-MRS). During incremental load, lactic acidosis was followed by a decline in intracellular pH. 31P-MRS studies has been definitely proved that this change in intracellular pH shows the threshold behavior. Some reports discussed the intracellular pH threshold (pHT) as an anaerobic threshold (AT) from the view point of intracellular events. However, our studies revealed that pHT did not reflect the onset of lactate production. In this article, studies of intracellular pH of working muscle were reviewed in relation to an anaerobic threshold.

Anaerobiosis↗

PubMed1996

Effects of cooling portions of the head on human thermoregulatory response.

Seven healthy young male students participated in this study. Each subject sat on a chair in an anteroom at 25 degrees C for 30 min and then entered a climatic chamber, controlled at 40 degrees C and R.H. 50%, and sat on a chair for 90 min. Cooling of frontal portion including the region around the eyes (FC), occipital portion (OC), and temporal portion (TC) began after 50 min of entering. An experiment without head cooling (NC) was also made for the control measurement. Thermal comfort and thermal sensation were improved by head cooling, but response was the same regardless of portion cooled. Although rectal temperature, mean skin temperature and heart rate showed no significant effect due to head cooling, forearm skin blood flow (FBF), sweat rate (SR), and body weight loss (delta Wt) had a tendency to be depressed. FBF in FC and TC decreased during head cooling, but that in OC and NC did not change significantly, while SR in FC was depressed. delta Wt showed total sweating to decrease by FC and TC, and FC to have greater inhibitory effect on sweating than OC. Thermal strain was evaluated by the modified Craig Index (I(s)). I(s) in FC decreased significantly more than in NC. Cooling of other portions of the head had no significant effect on I(s). Cooling of the frontal portion of the head may thus be concluded to have the most effect on thermoregulatory response in a hot environment.

Acclimatization↗

PubMed1996

Magnetic resonance imaging of brain death.

Fifteen patients with clinical diagnosis of brain death were examined by magnetic resonance (MR) imaging. Aortography with intraarterial digital subtraction angiography (IADSA) was also performed in nine patients. MR imaging indications of the flow void phenomenon were evaluated in the cavernous portion of internal carotid artery (ICA) and the middle or anterior cerebral artery, and compared with the IADSA findings. The relative intensities of gray and white matters were also measured. MR imaging showed that flow voids were absent in the ICA in all eight patients in whom non-filling was confirmed by IADSA. In one patient, IADSA demonstrated intracranial flow despite the diagnosis of brain death and the flow void pattern was normal. Serial MR imaging showed disappearance or abnormality of flow voids after brain death in six patients and absence before brain death in one. Spotty flow voids became visible in the unilateral ICA of one case after brain death. Partial residual flow voids may be caused by to-and-fro blood movement which was demonstrated by transcranial Doppler sonography. The normal flow void pattern was seen in none of these patients, therefore absence of flow voids indicates cessation of intracranial blood flow. Proton density and T2-weighted MR images showed dissociated intensity changes between white and gray matters, which were thought to be characteristic of brain death. In conclusion, MR imaging can achieve non-invasive diagnosis of the non-filling phenomenon in patients with brain death.

Adult↗