《白色病》的危机主题

面对法西斯主义阴影笼罩下的世界,卡·恰佩克在戏剧《白色病》中描绘了这样一幅场景:一种名为“白色病”的病毒席卷人间,医生无计可施,政府无所作为,元帅发动的侵略战争更为这悲惨人间增添了残酷。本文以《白色病》为研究对象,以疾病为切入点分析作品中体现的生存焦虑,从生态危机,信仰危机及伦理危机等三个方面对作品的主题进行研究,解读满目疮痍的世界对人的压抑和规训,总结作品所暴露的社会问题,揭示恰佩克戏剧的道德教化功能。

论墨白小说中的病态人格——以《局部麻醉》和《白色病室》为例

医院是当下我们叩问生命的本质和意义、审视一种文化之于生命的关怀或扭曲的最合适的地方。墨白的两部以医院为题材的中篇小说《局部麻醉》和《白色病室》分别通过外科医生白帆和内科医生苏警己的视野和遭遇,呈现和揭示了罪恶的、病态的文化是怎样残酷地对人的身体和精神进行扭曲、规训和惩罚,驱迫生命走向疯狂和死亡的。

Genome Analysis in Wheat Breeding for Disease Resistance

A brief review on the development of wheat germplasm with introduced powdery mildew and scab resistance from Haynaldia villosa Sch. and Leymus racemosus Lam., Roegneria ciliaris (Trin.) Nevski as well as R. kamoji C. Koch respectively was made. In the course of germplasm development, genome analysis by means of chromosome banding, genomic in situ hybridization (GISH) or fluorescence in situ hybridization (FISH), molecular markers, particularly restriction fragment length polymorphism (RFLP) coupled with aneuploid analysis was employed for the purpose of improving breeding efficiency. Potential use of such germplasm in wheat breeding practice, basic studies and some related problems were also discussed.

The Gene of Megalencephalic Leukoencephalopathy with Subcortical Cysts is Mapped on Chromosome 22q13.3 with 250 kb Interval

Objective: Vacuolating megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a recently described syndrome with autosomal recessive mode of inheritance. Its possible gene was located on chromosomal 22q tel with 3-cM. The purpose of this study was to narrow down the genetical distance on chromosomal 22q tel with MLC. Methods: Thirty-nine MLC patients in 33 families were collected,and the linkage analysis and haplotype analysis of twelve informative families were done, using seven microsatellite markers and four SNP markers. Results: The maximum tow-point LOD score for marker 355c18 was 6.65 at recombination fraction 0.02. The haplotype analysis narrowed down the critical region of MLC to 250 kb on chromosomal 22q tel. Conclusion: One of the causing genes of MLC was located on chromosomal 22q tel with 250 kb. Four candidate genes were considered. The heterogeneity of one informative family indicated possible existence of a second locus for MLC.

Induction of apoptosis by shikonin through a ROS/JNK-mediated process in Bcr/Abl-positive chronic myelogenous leukemia （CML） cells

This study examined the signaling events induced by shikonin that lead to the induction of apoptosis in Bcr/ Abl-positive chronic myelogenous leukemia （CML） cells （e.g., K562, LAMA84）. Treatment of K562 cells with shikonin （e.g., 0.5 pM） resulted in profound induction of apoptosis accompanied by rapid generation of reactive oxygen species （ROS）, striking activation of c-Jun-N-terminal kinase （JNK） and p38, marked release of the mitochondrial proteins cytochrome c and Smac/DIABLO, activation of caspase-9 and -3, and cleavage of PARP. Scavenging of ROS completely blocked all of the above-mentioned events （i.e., JNK and p38 phosphorylation, cytochrome c and Smac/DIABLO release, caspase and PARP cleavage, as well as the induction of apoptosis） following shikonin treatment. Inhibition of JNK and knock-down of JNK1 significantly attenuated cytochrome c release, caspase cleavage and apoptosis, but did not affect shikonin-mediated ROS production. Additionally, inhibition of caspase activation completely blocked shikonin-induced apoptosis, but did not appreciably modify shikonin-mediated cytochrome c release or ROS generation. Altogether, these findings demonstrate that shikonin-induced oxidative injury operates at a proximal point in apoptotic signaling cascades, and subsequently activates the stress-related JNK pathway, triggers mitochondrial dysfunction, cytochrome c release, and caspase activation, and leads to apoptosis. Our data also suggest that shikonin may be a promising agent for the treatment of CML, as a generator of ROS.

Distribution and ultrastructure of pigment cells in the skins of normal and albino adult turbot, Scophthalmus Maximus

The distribution and ultrastructure of pigment cells in skins of normal and albino adult turbots were examined with transmission electron microscopy （TEM）. Three types of pigment cells of melanophore, iridophore and xanthophore have been recognized in adult turbot skins. The skin color depends mainly on the amount and distribution of melanophore and iridophore, as xanthophore is quite rare. No pigment cells can be found in the epidermis of the skins. In the pigmented ocular skin of the turbot, melanophore and iridophore are usually co-localized in the dermis. This is quite different from the distribution in larvae skin. In albino and white blind skins of adult turbots, however, only iridophore monolayer still exists, while the melanophore monolayer disappears. This cytological evidence explains why the albino adult turbot, unlike its larvae, could never resume its body color no matter what enviroumental and nutritional conditions were provided. Endocytosis is quite active in the cellular membrane of the iridophore. This might be related to the formation of reflective platelet and stability of the iridophore.

The Potential Role of Powdery Mildew-Resistance Gene Pm40 in Chinese Wheat-Breeding Programs in the Post-Pro21 Era

Powdery mildew, which is caused by Blumeria graminis f. sp. tritici （Bgt）, is an important leaf disease that affects wheat yield. Powdery mildew-resistance （Pro） gene Pro21 was first transferred into wheat in the 1980s, by translocating the Heuchera villosa chromosome arm 6VS to the wheat chromosome arm 6AL （6VS.6AL）. Recently, new Bgt isolates that are virulent to Pm21 have been identified in some wheat fields, indicating that wheat breeders should be aware of the risk of deploying Pm21, although pathological details regarding these virulent isolates still remain to be discovered. Pm40 was identified and mapped on the wheat chromosome arm 7BS from several wheat lines developed from the progenies of a wild cross between wheat and Thinopyrum intermedium. Pm40 offers a broad spectrum of resistance to Bgt, which suggests that it is likely to provide potentially durable resistance. Cytological methods did not detect any large alien chromosomal segment in the wheat lines carrying Pm40. Lines with Pm40 and promising agronomical traits have been released by several wheat-breeding programs in the past several years. Therefore, we believe that Pm40 will play a role in powdery mildew-resistance wheat breeding after Pm21 resistance is overcome by Bgt isolates. In addition, both Prn21 and Pm40 were derived from alien species, suggesting that the resistance genes derived from alien species are potentially more durable or effective than those identified from wheat.

A novel t(3;12)(q21;p13) translocation in a patient with accelerated chronic myeloid leukemia after imatinib and nilotinib therapy

The acquisition of secondary chromosomal aberrations in chronic myeloid leukemia (CML) patients with Philadelphia chromosome-positive (Ph+) karyotype signifies clonal evolution associated with the progression of the disease to its accelerated or blastic phase. Therefore, these aberrations have clinical and biological significance. T(3;12)(q26;p13), which is a recurrent chromosomal aberration observed in myeloid malignancies, is typically associated with dysplasia of megakaryocytes, multilineage involvement, short duration of any blastic phase, and extremely poor prognosis. We have identified a recurrent reciprocal translocation between chromosomes 3 and 12 with different breakpoint at bands 3q21 in the malignant cells from a 28-year-old man. The patient was initially diagnosed as having Ph+ CML in the chronic phase. The t(3;12)(q21;p13) translocation occurred 4 years after the patient was first diagnosed with CML while undergoing tyrosine kinase inhibitor therapy. We confirmed the t(3;12)(q21;p13) translocation via fluorescence in situ hybridization assay by using whole-chromosome paint probes for chromosomes 3 and 12. Our findings demonstrate that, similar to other recurrent translocations involving 3q26 such as t(3;3) and t(3;21), the t(3;12)(q21;p13) translocation is implicated not only in myelodysplastic syndrome and acute myeloid leukemia but also in the progression of CML. These findings extend the disease spectrum of this cytogenetic aberration.

ONE CASE OF LEUKEMIA INDUCED BY ^(60)Co ACCIDENT

The peripheral blood lymphocyte chromosomes in a case of 60Co γ rays accident were examined at 2.5h after exposure. The frequency of the dicentrics plus centric rings was 89% and exposure dose was estimated to be 4.78 (4.53～4.88) Gy. The examinations of lymphocyte chromosome aberration within follow-up 12α showed that the incidence of Dic+R reduced with lg regression (r = -0.9895). While the number of cells with stable aberration remained unchanged and showed a tendency to increase. During the period of leukemia, bone marrow cell chromosome aberrations were studied by method of G-banding. Of 13 cells observed, 4 cells belonged to normal karyotypes. Among 9 aberration cells, 12 aberrations were detected. The majority of which were classified as translocation, deletion and inversion. Numeric aberrations were-9,-12,-20,-22,-y. This case suggested that acute lymphocytic leukemia was induced after radiation accident.

Establishment and Characterization of a New Cell Line from the Kidney of Spotted Halibut Verasper variegates

A cell line, SHK, was derived from the kidney of spotted halibut Verasper variegates. The cell line was subcultured more than 40 passages in minimum essential medium （MEM） supplemented with fetal bovine serum （FBS） and 10 ng ml4 basic fibroblast growth factor （bFGF）. Cell morphology from primary culture and subculture was observed continuously by microscopy. The SHK cell line consisted predominantly of fibroblast-like cells. The cell line was able to grow between 20℃ and 30℃ with the optimum growth at 24℃ and with a reduced growth between 12℃ and 20℃. The growth rate of the cells increased as the proportion of FBS increased from 10% to 20% at 28℃ with optimum growth at the concentration of 20%. The doubling time of the cells was determined to be 44.8 h. Chromosome analysis revealed that 52% of the SHK cells maintained a normal diploid chromosome number （2n=46）. The cells were successfully transfected with green fluorescent protein （GFP） reporter plasmids and the expression of GFP gene in the cells indicated the possible utility of the cells in gene expression studies. The cells were infected by lymphosystis disease virus （LCDV） and found to be susceptible to the virus in cytopathic effect （CPE） observation. The infection was confirmed by PCR and electron microscopy experiments, which proved the existence of the viral particles in the cytoplasm of the virus-infected cells.

The Application of Spectral Karyotyping in Leukemia

Spectral karyotyping (SKY) is a novel cytogenetic technique, which has been developed to unambiguously display and identify all 24 human chromosomes at one time without previous knowledge of any abnormalities involved. SKY can discern aberrations that fail to be easily detected by conventional banding techniques and by fluorescent in situ hybridization (FISH). Therefore SKY is highly accurate, highly sensitive, and highly prognostic. In this report the featurese and application of SKY in studies of leukemia are reviewed.

TAT Improves in vitro Transportation of Fortilin Through Midgut and into Hemocytes of White Shrimp Litopenaeus vannamei

Fortilin is a multifunctional protein implicated in many important cellular processes. Since injection of Pm-fortilin reduces shrimp mortality caused by white spot syndrome virus (WSSV), there is potential application of fortilin in shrimp culture. In the present study, in order to improve trans-membrane transportation efficiency, the protein transduction domain of the transactivator of transcription (TAT) peptide was fused to fortilin. The Pichia pastoris yeast expression system, which is widely accepted in animal feeds, was used for production of recombinant fusion protein. Green fluorescence protein (GFP) was selected as a reporter because of its intrinsic visible fluorescence. The fortilin, TAT and GFP fusion protein were constructed. Their trans-membrane transportation efficiency and effects on immune response of shrimp were analyzed in vitro. Results showed that TAT peptide improved in vitro uptake of fortilin into the hemocytes and midgut of Litopenaeus vannamei. The phenoloxidase (PO) activity of hemocytes incubated with GFP-Fortilin or GFP-Fortilin-TAT was significantly increased compared with that in the control without expressed fortilin. The PO activity of hemocytes incubated with 200 μg mL-1 GFP-Fortilin-TAT was significantly higher than that in the group with the same concentration of GFP-Fortilin. Hemocytes incubated with GFP-Fortilin-TAT at all concentrations showed significantly higher nitric oxide synthase (NOS) activity than those in the control or in the GFP-Fortilin treatment. The present in vitro study indicated that TAT fusion protein improved the immune effect of fortilin.

Autosomal dominant polycystic liver disease in a family without polycystic kidney disease associated with a novel missense protein kinase C substrate 80K-H mutation

Polycystic liver disease (PLD) is characterized by the presence of multiple bile duct-derived epithelial cysts scattered in the liver parenchyma. PLD can manifest itself in patients with severe autosomal dominant polycystic kidney disease (ADPKD). Isolated autosomal dominant polycystic liver disease (ADPLD) is genetically distinct from PLD associated with ADPKD, although it may have similar pathogenesis and clinical manifestations.Recently, mutations in two causative genes for ADPLD,independently from ADPKD, have been identified. We report here a family (a mother and her daughter) with a severe form of ADPLD not associated with ADPKD produced by a novel missense protein kinase C substrate 80K-H (PRKCSH) mutation (R281W). This mutation causes a severe phenotype, since the two affected subjects manifested signs of portal hypertension. Doppler sonography, computed tomography (CT) and magnetic resonance (MR) imaging are effective in documenting the underlying lesions in a non-invasive way.

Differences in MITF gene expression and histology between albino and normal sea cucumbers (Apostichopus japonicus Selenka)

Albino Apostichopus japonicus occur both in the wild and in captivity. The offspring of albino A. japonicus also suffer from albinism. The formation of melanin in the melanocytes is dependant on microphthalmia-associated transcription factor (MITF). To investigate the role of MITF in controlling albinism, we cloned the full-length MITF cDNA from A. japonicus and compared MITF mRNA expression in albino and normal A. japonicus. In addition, we used light and electron microscopy to compare histological samples of normal and albino A. japonicus. The body wall of albino adults was characterized by significantly lower levels of MITF expression and lower numbers of epidermal melanocytes, which also contained less melanin. In albino juvenile offspring, MITF expression levels were significantly lower 32 d after fertilization and there were fewer, and less developed, epidermal melanocytes. Thus, we conclude that albino A. japonicus have fewer melanocytes and a reduced ability to synthesize melanin, likely because of lower expression of MITF.

Function of the hemochromatosis protein HFE:Lessons from animal models

Hereditary hemochromatosis （HH） is caused by chronic hyperabsorption of dietary iron. Progressive accumulation of excess iron within tissue parenchymal cells may lead to severe organ damage. The most prevalent type of HH is linked to mutations in the HFE gene, encoding an atypical major histocompatibility complex class I molecule. Shortly after its discovery in 1996, the hemochromatosis protein HFE was shown to physically interact with transferrin receptor 1 （TfR1） and impair the uptake of transferrin-bound iron in cells. However, these findings provided no clue why HFE mutations associate with systemic iron overload. It was later established that all forms of HH result from misregulation of hepcidin expression. This liverderived circulating peptide hormone controls iron efflux from duodenal enterocytes and reticuloendothelial macrophages by promoting the degradation of the iron exporter ferroportin. Recent studies with animal models of HH uncover a crucial role of HFE as a hepatocyte iron sensor and upstream regulator of hepcidin. Thus, hepatocyte HFE is indispensable for signaling to hepcidin, presumably as a constituent of a larger ironsensing complex. A working model postulates that the signaling activity of HFE is silenced when the protein is bound to TfR1. An increase in the iron saturation of plasma transferrin leads to displacement of TfR1 from HFE and assembly of the putative iron-sensing complex. In this way, iron uptake by the hepatocyte is translated into upregulation of hepcidin, reinforcing the concept that the liver is the major regulatory site for systemic iron homeostasis, and not merely an iron storage depot.

Survival of the biocontrol agents Brevibacillus brevis ZJY-1 and Bacillus subtilis ZJY-116 on the spikes of barley in the field

Fusarium head blight (FHB) caused by Fusarium graminearum is a devastating disease that results in extensive yield losses to wheat and barley. A green fluorescent protein (GFP) expressing plasmid pRP22-GFP was constructed for monitoring the colonization of two biocontrol agents, Brevibacillus brevis ZJY-1 and Bacillus subtilis ZJY-116, on the spikes of barley and their effect on suppression of FHB. Survival and colonization of the Brevibacillus brevis ZJY-1 and Bacillus subtilis ZJY-116 strains on spikes of barley were observed by tracking the bacterial transformants with GFP expression. Our field study revealed that plasmid pRP22-GFP was stably maintained in the bacterial strains without selective pressure. The retrieved GFP-tagged strains showed that the bacterial population fluctuation accorded with that of the rain events. Furthermore, both biocontrol strains gave significant protection against FHB on spikes of barley in fields. The greater suppression of barley FHB disease was resulted from the treat-ment of barley spikes with biocontrol agents before inoculation with F. graminearum.

S-1 induced secondary acute erythroid leukemia with a chromosome inv(12)(p13;q13)

Adjuvant chemotherapy by S-1 following gastrectomy is considered standard treatment in Japan.Analysis of follow-up data have proved the effi cacy of S-1 admin-istration,and that hematological adverse events were relatively rare.Pyrimidine anti-metabolites,including S-1,have shown relatively lower risks for secondary hematological malignancies in comparison to alkylat-ing agents and topoisomerase-Ⅱ inhibitors.We here report a case of therapy-related leukemia after S-1 administration.A patient who had received S-1as the sole adjuvant chemotherapy was diagnosed with acute erythroid leukemia.To the best of our knowledge,our patient represents the fi rst report of S-1 induced acute leukemia.

Atypical Chronic Myeloid Leukaemia with Trisomy 13: a Case Report

ATYPICAL chronic myeloid leukaemia （aCML）, which shows both myeloproliferative and mye- Iodysplastic features, is a type of myeloprolif- erative/myelodysplastic disease as defined bythe World Health Organisation （WHO） classification of the myeloid neoplasms. Because of the presence of neutrophilic leukocytosis, aCML may resemble chronic myeIogenous leukemia （CML）. However, in contrast with CML, aCML does not have the Philadelphia chromosome or the bcr/abl fusion gene.

Hereditary pancreatitis

Hereditary pancreatitis is an autosomal dominant condition,which results in recurrent attacks of acute pancreatitis,progressing to chronic pancreatitis often at a young age.The majority of patients with hereditary pancreatitis expressone of two mutations (R122H or N29I) in the cationictrypsinogen gene (PRSS1 gene). It has been hypothesisedthat one of these mutations, the R122H mutation causespancreatitis by altering a trypsin recognition site sopreventing deactivation of trypsin within the pancreas andprolonging its action, resulting in autodigestion. Families withthese two mutations have been identified in many countriesand there are also other rarer mutations, which have alsobeen linked to hereditary pancreatitis.Patients with hereditary pancreatitis present in the sameway as those with sporadic pancreatitis but at an earlierage. It is common for patients to remain undiagnosed formany years, particularly ifthey present with non-specificsymptoms. Hereditary pancreatitis should always beconsidered in patients who present with recurrent pancreatitiswith a family history of pancreatic disease. If patients withthe 2 common mutations are compared, those with theR122H mutation are more likely to present at a younger ageand are more likely to require surgical intervention than thosewith N29I. Hereditary pancreatitis carries a 40 % lifetimerisk of pancreatic cancer with those patients aged between50 to 70 being most at risk in whom screening tests maybecome important.

In Vivo Kinetics and Biodistribution of a Hantaan Virus DNA Vaccine after Intramuscular Injection in Mice

To study the kinetics in vivo of a Hantaan virus DNA vaccine, we constructed a fusion DNA vaccine, pEGFP/S, by cloning the S segment of Hantavirus into the vector, pEGFP-C1, which encodes Green fluorescent protein EGFP. In this report, we provide evidence that pEGFP/S was distributed and persistently expressed for more than 60 days in several organs after inoculation. Our findings suggest that the persistent immune responses induced by a Hantaan virus DNA vaccine are likely due to the plasmid pEGFP/S deposited in vivo, which acts as a booster immunization.