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91.
92.
Noninvasive investigation of exocrine pancreatic function: Feasibility of cine dynamic MRCP with a spatially selective inversion‐recovery pulse 下载免费PDF全文
93.
94.
95.
Lymphomatoid Granulomatosis with Central Nervous System Involvement Successfully Treated with Cyclophosphamide,High‐dose Cytarabine,Dexamethasone, Etoposide,and Rituximab (CHASER therapy) Followed by Brain Irradiation: A Case Study 下载免费PDF全文
96.
We compared the growth of 183 children with short stature (≤ 2SD) and 73 children of
normal height at age six who were visiting the Tanaka Growth Clinic. We classified these
short children as suffering from either idiopathic short stature (ISS, n = 119), GH
deficiency (GHD, n = 33) or small-for-gestational-age short stature (SGASS, n = 31) on the
basis of subsequent test results and other factors. We also conducted a retrospective
study of changes in their height, wt and nutritional intake over time. The mean changes in
height SD score from birth to 6 yr were –0.24 SD in normal height children with a normal
birth length and +2.27 SD in normal height children with a low birth length. In short
children, these changes were –1.93 SD for children with ISS, –2.41 SD for those with GHD
and +0.58 for those with SGASS. The mean changes from birth to 6 mo were –0.84 SD, −1.03
SD and +0.38 SD in children with ISS, GHD and SGASS, respectively. The mean change in
height SD score from birth to age 1 yr was –1.07 SD, –1.44 SD and +0.35 SD, respectively.
The decrease in height SD score from birth to 6 mo accounted for 43.5% of the decrease in
height SD score from birth to 6 yr in children with ISS and it accounted for 42.6% of the
decrease in children with GHD. Only 19% of short children bottle-fed well, and 53% fed
poorly, as opposed to 56% and 16% of normal height children who fed well and poorly,
respectively. Post weaning, only 22% of short children ate well, and 56% fed poorly, as
opposed to 53% and 17% of normal height children who fed well and poorly, respectively.
These findings demonstrated that growth failure started from early infancy in ISS and GHD
children. It was suggested that poor nutritional intake in infancy and early childhood was
a partial cause of short stature at age 6. 相似文献
97.
Summary The role of Ca2+ release channels in the sarcoplasmic reticulum in modulating physiological automaticity of the sinoatrial (SA) node was studied by recording transmembrane action potentials and membrane ionic currents in small preparations of the rabbit SA node. Ryanodine, which modifies the conductance and gating behavior of the Ca2+ release channels, was used to block Ca2+ release from the sarcoplasmic reticulum. Superfusion of 1-mM ryanodine decreased the spontaneous firing frequency as well as the maximal rate of depolarization of the SA, and these reductions reached a steady state within approximately 5min. The action potential recordings revealed that the latter part of diastolic depolarization was depressed and that the take-off potential became less negative. This suggested that the negative chronotropic effect of ryanodine resulted from the blockade of physiological Ca2+ release from the sarcoplasmic reticulum. In voltage clamp experiments, using double-microelectrode techniques, ryanodine did not markedly reduce the Ca2+ current (ICa) but decreased the delayed rectifying K+ current (IK), the steady-state inward current (Iss), and the hyperpolarization-activated inward current (Ih). These observations suggest that, even when the function of Ca2+ channels in the cell membrane is normally maintained, depression of Ca2+ release channels in the sarcoplasmic reticulum would prevent sufficient elevation of the Ca2+ concentration in SA node cells for the activation of various ionic currents, and, thus adversely affect the physiological automaticity of this primary cardiac pacemaker. 相似文献
98.
Shirato K Morimoto M Tomita N Kokawa A Sugimori K Saito T Tanaka K 《Hepato-gastroenterology》2002,49(46):897-899
A 2.5-cm diameter, exophytic seeding of hepatocellular carcinoma was detected by contrast-enhanced computed tomography in a 76-year-old man. He had previously undergone a radiofrequency ablation therapy with an expandable, ten-hook needle electrode for the treatment of a 1.5-cm hepatocellular carcinoma in liver segment VI. Ultrasound-guided fine needle biopsy revealed that this hepatocellular carcinoma was moderately differentiated, as initial tumor was. An additional radiofrequency ablation achieved complete ablation of this neoplastic mass on contrast-enhanced computed tomography scanning. Recurrences were not found for eight months after. To prevent tumor seeding, using thermocoagulation when retracting the needle electrode may be useful. 相似文献
99.
Okamoto M Ohara-Imaizumi M Kubota N Hashimoto S Eto K Kanno T Kubota T Wakui M Nagai R Noda M Nagamatsu S Kadowaki T 《Diabetologia》2008,51(5):827-835
Aims/hypothesis A decrease in plasma adiponectin levels has been shown to contribute to the development of diabetes. However, it remains uncertain
whether adiponectin plays a role in the regulation of insulin secretion. In this study, we investigated whether adiponectin
may be involved in the regulation of insulin secretion in vivo and in vitro.
Methods The effect of adiponectin on insulin secretion was measured in vitro and in vivo, along with the effects of adiponectin on
ATP generation, membrane potentials, Ca2+ currents, cytosolic calcium concentration and state of 5′-AMP-activated protein kinase (AMPK). In addition, insulin granule
transport was measured by membrane capacitance and total internal reflection fluorescence (TIRF) analysis.
Results Adiponectin significantly stimulated insulin secretion from pancreatic islets to approximately 2.3-fold the baseline value
in the presence of a glucose concentration of 5.6 mmol/l. Although adiponectin had no effect on ATP generation, membrane potentials,
Ca2+ currents, cytosolic calcium concentrations or activation status of AMPK, it caused a significant increase of membrane capacitance
to approximately 2.3-fold the baseline value. TIRF analysis revealed that adiponectin induced a significant increase in the
number of fusion events in mouse pancreatic beta cells under 5.6 mmol/l glucose loading, without affecting the status of previously
docked granules. Moreover, intravenous injection of adiponectin significantly increased insulin secretion to approximately
1.6-fold of baseline in C57BL/6 mice.
Conclusions/interpretation The above results indicate that adiponectin induces insulin secretion in vitro and in vivo.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorised users.
M. Okamoto and M. Ohara-Imaizumi contributed equally to this study. 相似文献
100.
Akihiro Nakamura Yuto Monma Shoko Kajitani Kazuki Noda Sota Nakajima Hideaki Endo Tohru Takahashi Eiji Nozaki 《Heart and vessels》2016,31(9):1446-1455
Both postprandial hyperlipidemia and hyperinsulinemia have been thought to play an important role in the development of atherosclerosis, and to be a potent risk factor for cardiovascular event. To examine effects of glycemic state on postprandial hyperlipidemia and hyperinsulinemia in patients with coronary artery disease (CAD), a total of 112 consecutive male patients with angiographically confirmed CAD were loaded with a high-fat and high-glucose test meal. CAD patients were divided into three groups as “non-diabetic”, “prediabetic”, and “diabetic” CAD groups. The serum triglyceride (TG) and remnant-like particle cholesterol (RLP-C) levels at the 6th hour in diabetic CAD group showed significantly higher than non-diabetic CAD group, and the incremental area under the curves (iAUCs) of these levels in diabetic CAD group were significantly greater than non-diabetic CAD group (TG, P = 0.0194; RLP-C, P = 0.0219). There were no significant differences in the iAUCs of TG or RLP-C between prediabetic and non-diabetic CAD group. The AUCs of plasma insulin levels or insulin resistance index (IRI): (AUCs of insulin) × (AUCs of glucose) as the insulin resistance marker were greater in diabetic CAD group than non-diabetic CAD group (insulin, P = 0.0373; IRI, P = 0.0228). The AUCs of serum TG or RLP-C levels showed a correlation with the AUCs of plasma insulin (AUC-TG, r = 0.5437, P < 0.0001; AUC-RLP-C, r = 0.6847, P < 0.0001), and they correlated well with the insulin resistance index (AUC-TG, r = 0.7724, P < 0.0001; AUC-RLP-C, r = 0.7645, P < 0.0001). We found that the insulin resistance showed a close relationship with postprandial hyperlipidemia in CAD patients. Diabetic, but not prediabetic state, may be a risk for postprandial impaired lipid metabolism in CAD patients. 相似文献