Serum lipids, lipoproteins and apolipoproteins in patients with senile dementia]

Serum lipid, lipoprotein, apolipoprotein, and sterol profiles were studied in 22 patients with senile dementia of the Alzheimer type (SDAT) and 29 patients with vascular dementia (VD). Levels of high density lipoprotein-cholesterol (HDL-C) were lower in both patients groups of SDAT and VD than in control group. Apolipoprotein AI and AII are two major proteins in HDL. In this study, apolipoprotein AI levels were normal, but apolipoprotein AII levels were lower in the patient groups, especially in the VD group, than in the control group. Lipoprotein(a) levels were higher in both patient groups, especially in the VD group. There were no differences of cholesterol, cholesterol precursors (desmosterol and lathosterol), and plant sterols (campesterol and beta-sitosterol) among the three groups. Murine apolipoprotein AII is a serum precursor of murine senile amyloid protein, and the apolipoprotein AII variant with proline-->glutamine substitution at position 5 in the serum of accelerated senescence-prone mice is identical to the murine senile amyloid fibril protein from amyloid-deposited tissues of these mice. In human SDAT and VD, the reason for the low level of apolipoprotein AII remains unclear.     

Local cerebral blood flow measured by stable xenon CT during fentanyl-diazepam anesthesia

We assessed the local cerebral blood flow (LCBF) in 40 patients under fentanyl-diazepam anesthesia. The measurement of LCBF was made using 50%–70% stable xenon with 20 min of inhalation interval and a shuttle method for computed tomography imaging. All patients were anesthetized with 5.95±1.76 μg·kg⁻¹ fentanyl and 0.22±0.07 mg·kg⁻¹ diazepam under mechanical ventilation during CBF measurement. The values and distribution of LCBF on non-affected hemisphere appeared to be unaltered by fentanyldiazepam anesthesia. We also assessed the cerebral carbon dioxide reactivity in 6 patients. The cerebral carbon dioxide reactivity, expressed as percentage change in LCBF per unit change in arterial carbon dioxide partial pressure, was 5.39±1.07, and there were no significant differences of reactivity among regions studied. In conclusion, we showed reference values of LCBF and carbon dioxide reactivity, measured by stable xenon-enhanced computed tomography, in patients under fentanyl-diazepam anesthesia. Carbon dioxide reactivity was preserved in all regions including gray matter, white matter, and basal ganglia.     

Bilateral symmetric tonic posturing suggesting propagation to the supplementary motor area in a patient with precuneate cortical dysplasia.

We report a patient manifesting seizures with bilateral symmetric tonic posturing, which were markedly reduced after resection of the left precuneus. A 16-year-old man had sudden onset, complex partial seizures with bilateral symmetric tonic posturing since the age of eight years. Magnetic resonance fluid-attenuated inversion-recovery imaging revealed a hyperintense lesion in left precuneus. In almost all focal seizures recorded during an invasive EEG evaluation, ictal onset was detected from the inferomesial aspect of the lesion, but fast paroxysmal discharges from the ipsilateral supplementary motor area (SMA) were observed just before the clinical onset. After surgical excision of the EEG onset zone, including the lesion, seizure frequency was markedly (> 95%) reduced. By the 20th month after surgery, there were only brief nocturnal seizures involving slight elevation of both shoulders and slight abduction of both arms, with preservation of consciousness occurring once every few days. Invasive EEG findings and surgical outcome suggested that the epileptic activity originating from the epileptogenic zone may have propagated to the symptomatogenic zone including mainly the ipsilateral SMA. In summary, we report an interesting case of bilateral symmetric tonic posturing suggesting propagation to the SMA. MRI and invasive EEG confirmed the epileptogenic focus as a precuneate cortical dysplasia lesion.[Published with video sequences].     

Media conditioned by smooth muscle cells cultured in a variety of hypoxic environments stimulates in vitro angiogenesis. A relationship to transforming growth factor-beta 1.

Conditioned media (CM) harvested from bovine smooth muscle cells (SMCs) of aortic media cultured under hypoxic conditions remarkably enhanced angiogenesis in vitro, that is, the tube formation of bovine capillary endothelial cells (BCEs) cultured on type I collagen gels. The extent of in vitro angiogenesis was assessed by the total length of tube structures formed by BCEs per area measured quantitatively with an image analyzer. The tube formation in CM obtained from the cultivation of SMCs at 1% O2 for 24 hours was enhanced by about 1.5 times and 3.4 times as compared with those at 5% O2 and 20% O2, respectively. This tube-forming activity was abrogated by the pretreatment of CM with anti-transforming growth factor (TGF)-beta 1 IgG, but not by anti-basic fibroblast growth factor IgG. The SMC-CM obtained from hypoxic cultivation (1% O2 for 24 hours) inhibited [3H] thymidine incorporation by BCEs, SMCs, and fibroblasts more than about 20% of control. Anti-TGF-beta 1 IgG thus significantly reduced the inhibitory effect of hypoxic SMC-CM on DNA synthesis of these cells. These results suggest that SMCs in a hypoxic state release active in vitro angiogenic factors into CM, and active TGF-beta 1 is closely related to the in vitro angiogenic enhancement of media conditioned by SMCs cultured in a hypoxic state.     

Effect of KC399, a newly synthesized K+ channel opener, on acetylcholine-induced electrical and mechanical activities in rabbit tracheal smooth muscle.

1. Effects of KC399, an opener of ATP-sensitive K+ channels were investigated on membrane potential, isometric force and intracellular Ca2+ ([Ca2+]i) mobilization induced by acetylcholine (ACh) in smooth muscle from the rabbit trachea. 2. In these smooth muscle cells, ACh (0.1 and 1 microM) depolarized the membrane in a concentration-dependent manner, KC399 (1-100 nM) hyperpolarized the membrane whether in the presence or absence of ACh. When the concentration of ACh was increased, the absolute values of the membrane potential induced by the maximum concentration of KC399 were less negative. 3. ACh (0.1 to 10 microM) concentration-dependently produced a phasic, followed by a tonic increase in both [Ca2+]i and force. KC399 (above 3 nM) lowered the resting [Ca2+]i and attenuated the ACh-induced phasic and tonic increases in [Ca2+]i and force, in a concentration-dependent manner. The magnitude of the inhibition was greater for the ACh-induced tonic responses than for the phasic ones. Nicardipine (0.3 microM), a blocker of the L-type Ca2+ channel, attenuated the ACh-induced tonic, but not phasic, increases in [Ca2+]i and force. KC399 further attenuated the ACh-induced tonic responses in the presence of nicardipine. 4. In beta-escin-skinned strips, Ca2+ (0.3-10 microM) produced a contraction in a concentration-dependent manner. KC399 (0.1 microM) had no effect on the Ca(2+)-force relationship in the presence or absence of ATP with GTP. However, at a very high concentration (1 microM), this agent slightly shifted the relationship to the right and attenuated the maximum Ca(2+)-induced contraction.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of left atrial automatic tachycardia successfully treated with aprindine

Electrocardiogram in a 15-year-old girl showed persistent supraventricular tachycardia at rates of 130 to 140 bpm. Electrophysiological study confirmed left atrial automatic tachycardia, which was transferred to sinus rhythm by intravenous infusion of aprindine (100 mg/10 min). Therefore, aprindine (60 mg/day) was administered orally, and neither recurrence of left atrial automatic tachycardia nor side effects were observed during subsequent follow-up period of 16 months.     

Plasma lipoprotein(a) levels and expression of the apolipoprotein(a) gene are dependent on the nucleotide polymorphisms in its 5'-flanking region.

The apolipoprotein(a) (apo[a]) gene encodes a protein component of lipoprotein(a) [Lp(a)] whose plasma levels vary widely among individuals. Hyper-Lp(a)-emia constitutes a risk factor for thromboembolic disease. We previously subclassified the apo(a) gene into four allelic types (A-D) by polymorphisms in the 5''-flanking region. To elucidate whether these polymorphisms affect the expression of apo(a), we measured plasma Lp(a) concentrations in vivo by ELISA and examined expression of the gene by an in vitro assay using its 5''-flanking region. Homozygotes of type C had significantly higher Lp(a) levels than those of type D. The relative expression of type C was also about three times higher than that of type D, which was consistent with the in vivo results. Deletion analysis revealed that the substitution of C by T (+93) led to negative regulation in expression of the gene, while the change of G to A (+121) led to positive regulation. These results indicate that the polymorphisms in the 5''-flanking region of the apo(a) gene affect the efficiency of its expression and, in part, play a role in regulating plasma Lp(a) levels.