Altered p53 expression in Epstein Barr virus positive T cell lymphomas.

Recent studies have suggested a probable association between Epstein-Barr virus (EBV) and nasal/nasopharyngeal T cell lymphomas but the role of oncogenes or tumor suppressor genes is poorly understood. We have studied the frequency of p53 expression and its relation to the EBV infection in 33 Korean patients with head and neck (H&N) lymphomas. All cases (23 B cell & 10 T cell) were immunostained for p53 protein using the mAb D07 (Novocastra) and the avidin biotin peroxidase method. EBER in situ hybridization was performed using a fluorescein conjugated EBV oligonucleotide probe (Dako). Among 33 lymphomas, 16 cases stained positively for p53 protein. P53 expression was frequent both in higher grade lymphomas and in advanced stage. Nine cases were EBER positive, EBER was more commonly found in T cell lymphomas than in B cell lymphomas (70% vs 8.7%). EBER positive lymphomas showed a higher frequency of p53 positivity than EBER negative lymphomas (78% vs 38%), although the difference was not statistically significant (p = 0.095). These findings indicate altered expression of p53 protein occurs in H&N lymphomas, especially in late event lymphoma progression and appears to play a role in the development of EBER positive T cell lymphomas.     

Na+ channel expression and neuronal function in the Na+/H+ exchanger 1 null mutant mouse

Mice lacking Na(+)/H(+) exchanger 1 (NHE1) suffer from recurrent seizures and die early postnatally. Although the mechanisms for seizures are not well established, our previous electrophysiological work has shown that neuronal excitability and Na(+) current density are increased in hippocampal CA1 neurons of these mutant mice. However, it is unknown whether this increased density is related to altered expression or functional regulation of Na(+) channels. In this work, we asked three questions: is the increased excitability limited to CA1 neurons, is the increased Na(+) current density related to an increased Na(+) channel expression, and, if so, which Na(+) channel subtype(s) is upregulated? Using neurophysiological, autoradiographic, and immunoblotting techniques, we showed that both CA1 and cortical neurons have an increase in membrane excitability and Na(+) current density; Na(+) channel density is selectively upregulated in the hippocampus and cortex (P < 0.05); and Na(+) channel subtype I is significantly increased in the hippocampus and Na(+) channel subtype II is increased in the cortex. Our results demonstrate that mice lacking NHE1 upregulate their Na(+) channel expression in the hippocampal and cortical regions selectively; this leads to an increase in Na(+) current density and membrane excitability. We speculate that neuronal overexcitability due to Na(+) channel upregulation in the hippocampus and cortex forms the basis of epileptic seizures in NHE1 mutant mice.     

NC在医院信息化建设中的研究与应用

本文对医院信息化建设中存在的问题进行分析研究，提出网络计算机（NETWORK COMPUTER）的解决方案。通过NC与PC在性能、适用性、性价比等方面的对比研究与测试。得出NC在医院信息管理中的高可用性。     

终板蛋白多糖的变化对颈椎间盘力学性能的影响

目的:通过测定退变颈椎间盘压缩性能的改变,同时观测软骨终板基质蛋白多糖(proteoglycan PG)的变化,为退变的椎间盘显现异常力学特性作一分子机制上的探讨。方法:将24只家兔随机分为对照组和模型组,模型组家兔保持45°低屈曲住5小时/次·天,取C5-6椎间盘进行生物力学测定;同时生化测定椎间盘终板糖胺多糖(glycosaminoglycan,GAG)总量、硫酸软骨素(chongdroitin sulphate,CS)和硫酸角质素(keratan sulphate,KS)比值和透明质酸(hyaluronic acid,HA)含量;总结分析颈椎间盘退变时基质各成分的系统变化及其对椎间盘力学性能的影响。结果:模型组终板抗压强度、断裂时的最大形变、终板基质蛋白多糖总含量、硫酸软骨素/硫酸角质素比值、透明质酸含量都低于对照组(P<0.05),并随造模进程的深入而减小。结论:长时间的应力不均状态,造成椎间盘终板材料力学特性改变;颈椎间盘基质蛋白多糖含量和成分改变是颈椎间盘生物力学性能减退的主要原因之一。     

Interdependent effect of angiotensin-converting enzyme and platelet-activating factor acetylhydrolase gene polymorphisms on the progression of immunoglobulin A nephropathy

In order to investigate the interdependent action of the insertion/deletion polymorphism of the angiotensin-converting enzyme (ACE) gene and polymorphism in exon 11 (C1136-->T; Ala379Val) of the platelet-activating factor acetylhydrolase (PAF-AH) gene, which encodes a functional antagonist of PAF, on the progression of immunoglobulin A (IgA) nephropathy, we analysed both polymorphisms in patients with primary IgA nephropathy, who were followed-up for longer than 3 years. During the follow-up (87.3 +/- 50.0 months), the disease progressed in 38 of the 191 patients (19.9%). The D allele of the ACE gene in the absence of the T allele of the PAF-AH gene did not affect the prognosis [odds ratio (OR), 3.6; 95% confidence interval (CI), 0.8-16.4] and neither did the T allele in the absence of the D allele (OR, 3.0; 95% CI, 0.4-24.2). However, the presence of both was a significant prognostic factor (OR, 6.6; 95% CI, 1.4-31.3). After adjusting for other risk factors, the presence of both proved to be an independent risk factor (OR, 4.5; 95% CI, 1.6-12.7). These results suggest that the interdependent effects of ACE and PAF-AH polymorphisms on the progression of IgA nephropathy might be more important than the effect of the individual polymorphisms.     

Molecular targets of dietary polyphenols with anti-inflammatory properties

There is persuasive epidemiological and experimental evidence that dietary polyphenols have anti-inflammatory activity. Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) have long been used to combat inflammation. Recently, cyclooxygenase (COX) inhibitors have been developed and recommended for treatment of rheumatoid arthritis (RA) and osteoarthritis (OA). However, two COX inhibitors have been withdrawn from the market due to unexpected side effects. Because conventional therapeutic and surgical approaches have not been able to fully control the incidence and outcome of many inflammatory diseases, there is an urgent need to find safer compounds and to develop mechanism-based approaches for the management of these diseases. Polyphenols are found in many dietary plant products, including fruits, vegetables, beverages, herbs, and spices. Several of these compounds have been found to inhibit the inflammation process as well as tumorigenesis in experimental animals; they can also exhibit potent biological properties. In addition, epidemiological studies have indicated that populations who consume foods rich in specific polyphenols have lower incidences of inflammatory disease. This paper provides an overview of the research approaches that can be used to unravel the biology and health effects of polyphenols. Polyphenols have diverse biological effects, however, this review will focus on some of the pivotal molecular targets that directly affect the inflammation process.     

X-linked severe combined immunodeficiency syndrome: the first Korean case with gamma c chain gene mutation and subsequent genetic counseling

X-linked severe combined immunodeficiency (X-SCID) is a rare, life-threatening immune disorder, caused by mutations in the gamma c chain gene, which encodes an essential component of the cytokine receptors for interleukin-2 (IL-2), IL-4, IL-7, IL-9, IL-15, and IL-21. A 13-month-old boy with recurrent infections who had reduced serum immunoglobulin levels and decreased numbers of CD3, CD16/56 cells was evaluated for gamma c chain gene mutation and protein expression. The patient had a C-to-T point mutation at nucleotide position 690, one of the hot spots, resulting in a single amino acid substitution of cysteine for arginine (R226C), as determined by direct sequencing and PCR-RFLP. The patient's mother was a heterozygous carrier. Percutaneous umbilical cord blood sampling was performed at the 6-month of gestation in a subsequent pregnancy. As the immunophenotype of the fetus showed an identical pattern, the pregnancy was terminated and genetic analysis of the abortus confirmed recurrence. This is the first report of the molecular diagnosis of X-SCID in Korea. Genetic analysis of the gamma c chain gene is useful for definite diagnosis and genetic counseling for X-SCID.     

Isometric and isokinetic torque curves at the knee joint

Isometric and isokinetic torques of bilateral quadriceps and hamstrings were measured with Isokinetic Rehabilitation and Testing System (Model No. Cybex 340) on 40 normal untrained subjects, 20 males and 20 females, ranging between the ages of 23 and 35 years. The mean peak isometric and isokinetic torque values of both muscle groups showed no significant differences between dominant (right) and nondominant (left) limbs in both sexes; however there were significant differences between the male and the female. As the angular velocity increased, the peak torque significantly decreased, and the point of peak torque output occurred significantly later in the range of motion for quadriceps and hamstrings (p less than 0.01). There were no significant changes in the hamstrings to quadriceps (H/Q) ratios as the angular velocity increased. However, there were significant differences of mean H/Q ratio between male and female (p less than 0.01). Height had significant positive correlation with peak isometric and isokinetic torques for both quadriceps and hamstrings (p less than 0.01). Weight was found to correlate significantly with peak isometric and isokinetic torques (p less than 0.01). The mean isometric torques were significantly higher than the mean isokinetic torques for any joint angles in both sexes (p less than .01).     

Amino acid differences in capsid protein, VP1, between diabetogenic and nondiabetogenic variants of encephalomyocarditis virus

The genes for the major capsid protein, VP1(1D), of both diabetogenic D variant (EMC-D) and nondiabetogenic B variant (EMC-B) of encephalomyocarditis virus were cloned by using two synthetic primers which are common to both EMC-D and EMC-B. The cloned genes were mapped for major restriction enzyme sites including AccI, BamHI, EcoRI, HincII, KpnI, PvuII, SstI, TaqI, and XbaI. Among those nine restriction enzyme sites, only the TaqI site distinguished EMC-D genome from the counterpart of EMC-B genome. The complete nucleotide sequences (831 bases) of the VP1 genes revealed five amino acid differences between the two variants. Three of the changes, at positions 41, 58, and 152, were Thr (EMC-B) to Ala (EMC-D). The additional two changes occurred at positions 63 [Gln (EMC-B) to Glu (EMC-D)] and 181 [Thr (EMC-B) to Ser (EMC-D)]. All of these amino acid changes were due to point mutations at the first base of each codon.