Effects of cerulenin on the endogenous fatty acid synthetic activity in squamous cell carcinoma of the oral cavity.

PURPOSES: Inhibition of cerulenin on the endogenous fatty acid synthetic activities of oral squamous cell carcinoma (OSCC) and normal oral mucosa was assayed. METHODS: Squamous cell carcinoma and normal oral mucosa were collected fresh from surgical specimens. The collected tissues were minced in RPMI 1640 and divided into 3 groups: cerulenin treated, dimethylsulfoxide treated, and control. The tissues were incubated in [1(2)-(14)C]acetic acid, sodium salt for the last 2.5 hours of the treatment at 37 degrees C in 5% CO(2). After labeling, total lipids were extracted and counted for (14)C by scintillation counting. RESULTS: Endogenous fatty acid synthetic activities of oral squamous cell caranoma in the cerulenin-treated group decreased by 19% at 1 hour, 64% at 2 hours, and 87% at 4 hours; remained nearly unchanged in the dimethylsulfoxide-treated group; and increased slightly in the control group. The oral mucosa tissues were only mildly affected by cerulenin in fatty acid synthesis. CONCLUSIONS: Cerulenin significantly inhibits fatty acid synthetic activity in squamous cell carcinoma and only mildly affected the oral mucosa, indicating that the fatty acid synthetic pathway may be exploited as a target for developing anticancer drugs.     

48例干扰素治疗慢性乙肝不良反应的观察及护理

重组α-2b干扰素是具有抗病毒和免疫调节作用的生物学调节活性物质。近年来，国外文献报道α-2b干扰素治疗慢性乙型病毒性肝炎(CAH—B)取得较好效果。特别是基因工程问世，使大量的高纯度干扰素应用于临床。现对48例慢性乙肝患者使用干扰素后的不良反应的观察与护理，报道如下。     

The CLDN5 locus may be involved in the vulnerability to schizophrenia.

The present study was designed to detect three single nucleotide polymorphisms (SNPs) located on 22q11 that was thought as being of particularly importance for genetic research into schizophrenia. We recruited a total of 176 Chinese family trios of Han descent, consisting of mothers, fathers and affected offspring with schizophrenia for the genetic analysis. The transmission disequilibrium test (TDT) showed that of three SNPs, rs10314 in the 3'-untranslated region of the CLDN5 locus was associated with schizophrenia (chi(2) = 4.75, P = 0.029). The other two SNPs, rs1548359 present in the CDC45L locus centromeric of rs10314 and rs739371 in the 5'-flanking region of the CLDN5 locus, did not show such an association. The global chi-square (chi(2)) test showed that the 3-SNP haplotype system was not associated with schizophrenia although the 1-df test for individual haplotypes showed that the rs1548359(C)-rs10314(G)-rs739371(C) haplotype was excessively non-transmitted (chi(2) = 5.32, P = 0.02). Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.     

Protein ubiquitination in postsynaptic densities after transient cerebral ischemia.

The mechanisms underlying neurologic deficits and delayed neuronal death after ischemia are not fully understood. In the present study, we report that transient cerebral ischemia induces accumulation of ubiquitinated proteins (ubi-proteins) in postsynaptic densities (PSDs). By immunoelectron microscopy, we demonstrated that ubi-proteins were highly accumulated in PSD structures after ischemia. On Western blots, ubi-proteins were markedly increased in purified PSDs at 30 minutes of reperfusion, and the increase persisted until cell death in the CA1 region after ischemia. In the resistant DG area, however, the changes were transient and significantly less pronounced. Deposition of ubi-proteins in PSDs after ischemia correlates well with PSD structural damage in the CA1 region as viewed by electron microscopy. These results suggest that the ubiquitin-proteasome system fails to repair and remove damaged proteins in PSDs. The changes may demolish synaptic neurotransmission, contribute to neurologic deficits, and eventually lead to delayed neuronal death after transient cerebral ischemia.     

Laryngeal tuberculosis: a review of 26 cases.

OBJECTIVES: To review the clinical characteristics of laryngeal tuberculosis. STUDY DESIGN: Retrospective case series. SUBJECTS AND METHODS: Medical records of 26 histopathology-confirmed cases in a tertiary medical center from 1992 to 2006. RESULTS: The female patients were significantly younger than male patients. Hoarseness is the most common symptom (84.6%) because true vocal fold is most commonly involved (80.8%). Infection usually involves unilateral (66.7%) and right-side larynx but multiple subsites of the larynx (57.7%). The appearance of the affected larynx may have mixed features and change before diagnosis. Laryngeal tuberculosis is usually misdiagnosed as laryngeal cancer, especially in patients with malignant signs such as enlarged cervical lymph nodes and vocal fold immobility. Chest film is better than sputum examinations for screening. CONCLUSION: We should be especially alert about TB infection when facing young female patients with unusual laryngeal lesions. Extensive laser excision before diagnosis should be avoided because after antituberculous treatment, prognosis is usually good and vocal fold immobility could be reversible.     

Effect of amyloid peptides on the increase in TrkA receptor expression induced by nicotine in vitro and in vivo

The ability of nicotine to induce a cytoprotective or neuroprotective action occurs through several down-stream mechanisms. One possibility is that the drug increases the expression of tyrosine kinase A (TrkA) nerve growth factor (NGF) receptors. Certain β-amyloid peptides (e.g., Aβ1–42) have been shown to bind with high affinity to α7 nicotinic receptors and thus interfere with a potentially neurotrophic influence. Treatment of differentiated PC-12 cells with nicotine produced a concentration-dependent increase in cell-surface TrkA receptors that occurred concomitantly with cytoprotection. The effect of nicotine was blocked by either of the α7 receptor antagonists α-bungarotoxin (α-BTX) or methyllycaconatine. The cytoprotective action of nicotine also was inhibited by pretreatment with 10–100 nM Aβ1–42. Nicotine also was administered (four injections of 30 μg, spaced evenly over 24 h) to rats by direct injection into a lateral cerebral ventricle. Brain TrkA expression was increased significantly in hippocampus and entorhinal cortex (up to 32% above control), with no changes found in cerebral cortex or hypothalamus. The nicotine-induced increases in TrKA expression in hippocampus and entorhinal cortex were significantly inhibited by 10 μg α-BTX or by 10 nmol Aβ1–42. Therefore, physiologically relevant concentrations of Aβ1–42 can prevent nicotine-induced TrkA receptor expression in brain regions containing cholinergic neurons susceptible to the neurotoxicity associated with Alzheimer’s disease.     

Examination of potential mechanism(s) of metallothionein induction by diethyl maleate.

Diethyl maleate (DEM) is a glutathione-depleting agent that can increase the levels of the sulfhydryl-rich protein metallothionein (MT) in liver. The purpose of the present study was to examine the mechanism(s) by which DEM increases mouse hepatic MT levels. DEM appears to be an indirect MT inducer as suggested by the lack of increase in MT levels when cultured mouse hepatocytes were exposed to DEM. Four possible mechanisms by which indirect MT inducers may cause an elevation in MT concentrations in liver were examined. Zn levels did not increase prior to the increase in hepatic MT, thus, a Zn redistribution to the liver is not the cause of the liver MT induction by DEM. The adrenal gland products were not required for MT induction in liver, as adrenalectomy did not abolish the increase in hepatic MT caused by DEM. The elevation in liver MT does not appear to be due solely to the decrease in liver glutathione (60%) in the initial hour after DEM, because phorone, which decreases liver glutathione (80%), produced only a fourfold increase in hepatic MT. Activation of macrophages does not seem to account for the rise in liver MT levels, as there was no increase in abundance of cytokine mRNAs for TNF-alpha, IL-1 beta, or IL-6 in the liver. These data suggest that the induction of hepatic MT by DEM does not occur in response to (1) an increase in liver Zn that precedes the increase in liver MT, (2) release of adrenal gland products, (3) decrease in liver glutathione, or (4) increased cytokine gene expression.     

MRI manifestations of peritoneal carcinomatosis.

Three cases of proved peritoneal carcinomatosis were examined by magnetic resonance imaging (MRI). Air was used to distend the entire gastrointestinal tract via an antegrade method. The findings included seedings along the small intestine, transverse and sigmoid colon, stellate pattern in the mesentery, plaque-like and bulky tumor masses in the mesentery and greater omentum, and focal thickenings along the right subdiaphragmatic parietal peritoneum. Stenosis caused by tumor encasement at the duodenojejunal junction and ileocolic anastomosis were first detected by MRI and later confirmed by barium studies. Ascites was present in all cases. One case showed ascites located only along the left paracolic gutter. This report shows that MRI is also able to demonstrate peritoneal carcinomatosis by using air as a gastrointestinal contrast medium.     

小儿氨基酸注射液治疗胎儿宫内发育迟缓的探讨

经临床鉴定静脉内注射小儿氨基酸对治疗胎儿宫内发育迟缓具有肯定效果。在Ｂ超监视下，使用小儿氨基酸的孕妇组于用药期间，胎儿生长参数ＢＰＤ和ＨＣ显著高于使用成人氨基酸的孕妇组。１０例足月娩出胎儿体重均达到甚至超过２．５ｋｇ。由此得出结论：使用小儿氨基酸注射液对于改善胎儿宫内发育迟缓优于成人氨基酸。     

Clinical observation of Qi deficiency syndrome in 72 patients with chronic obstructive pulmonary disease treated with Yiqi Mianyi Granule

Seventy-two patients of chronic obstructive pulmonary disease (COPD) of Qi deficiency syndrome with abnormal immune indices were treated with Yiqi Mianyi Granule (YQMYG) and the efficacy was compared with that of 30 cases treated with Zhenqi fuzheng Granule (ZQFZG) for control. Results showed that the markedly effective rate of symptomatic improvement of Qi deficiency in YQMYG group was 65.3%, the total effective rate 93.1%. 88.6% of the immune indices lower than normal were corrected and 43. 7% of them were normalized, while for indices that were higher than normal the rate were 78.2% and 52.9% respectively. These results suggested that YQMYG could improve symptom of Qi Deficiency markedly, strengthen cellular immunity and regulate immune dysfunction. Its therapeutic efficacy was obviously superior to ZQFZG (P<0.Q5).