A Case of Cephalic Tetanus with Unilateral Ptosis and Facial Palsy

Cephalic tetanus is defined as a combination of trismus and paralysis of one or more cranial nerves. Cranial nerves III, IV, VI, VII, and XII may be affected, but the facial nerve is most frequently implicated. A 64-year-old female visited hospital for left ptosis followed by facial palsy after a left forehead abrasion in a car accident. At nine days post injury, left ptosis developed, left facial palsy developed twelve days post injury, and at fifteen days post injury, trismus and dysphagia developed. The following day, there was progression of symptoms to generalized tetanus, such as dyspnea and generalized rigidity. Videofluoroscopic swallow study showed penetration and aspiration. We report a case of cephalic tetanus with ptosis, facial palsy, and dysphagia, which progressed to generalized tetanus.

Collet-Sicard Syndrome in a Patient with Jefferson Fracture

Collet-Sicard syndrome is a rare condition characterized by the unilateral paralysis of the 9th through 12th cranial nerves. We describe a case of a 46-year-old man who presented with dysphagia after a falling down injury. Computed tomography demonstrated burst fracture of the atlas. Physical examination revealed decreased gag reflex on the left side, decreased laryngeal elevation, tongue deviation to the left side, and atrophy of the left trapezius muscle. Videofluoroscopic swallowing study (VFSS) revealed frequent aspirations of a massive amount of thick liquid and incomplete opening of the upper esophageal sphincter during the pharyngeal phase. We report a rare case of Collet-Sicard syndrome caused by Jefferson fracture.

Effect of Stimulation Intensity and Location of Cerebral Infarction on Motor Evoked Potentials in the Rat

OBJECTIVE: To investigate the change of motor evoked potential (MEP) in the cerebral infarction, and observe the effect of stimulation intensity and location of cerebral infarction, using rat model of cerebral ischemia induced by endothelin-1 (ET-1). METHOD: Middle cerebral artery (MCA) infarct, cortical infarct, and internal capsular infarct were induced in Spraugue-Dawley rats, by injecting ET-1 stereotaxically. MEP was recorded in forelimb by transcranial magnetic stimulation at 100%, 120%, and 150% of motor threshold by a small figure-8 coil. The location of cerebral infarction was confirmed histologically by 2,3,5-triphenyltetrazolium chloride (TTC) staining. RESULTS: In MCA infarct, MEP was not recorded at all intensity. In internal capsular infarct, no MEP was recorded at 100% of motor threshold, and amplitude was decreased at 120%. In cortical infarct, MEP was not recorded at 100%, but amplitude was maintained at 120% and 150%. Latency did not change significantly at all intensity. CONCLUSION: Amplitude of MEP decreased after cerebral infarction, but latency did not change. Decrease in amplitude was larger with deeper location of cerebral infarction. Cerebral cortex was stimulated at 100% of motor threshold, subcortical structure was stimulated at 120%, and deeper structure was stimulated at 150%, respectively.

Synergistic growth inhibition by combination of adenovirus mediated p53 transfer and cisplatin in ovarian cancer cell lines / 부인종양

OBJECTIVE: This study was to investigate the synergistic growth inhibitory effect by combination of adenovirus mediated p53 gene transfer and cisplatin in ovarian cancer cell lines with different p53 gene mutation patterns. METHODS: Three ovarian cancer cell lines, p53 deleted SKOV3, p53 mutated OVCAR-3, and PA-1 with wild-type p53 were transduced with human adenovirus vectors carrying p53 gene (Ad-p53) and treated with a sublethal concentration of cisplatin before and after Ad-p53. The cell number was counted daily for 5 days after Ad-p53 transduction. Western blotting was used to identify p53 and p21 protein expressions, and flow cytometric analysis was performed to investigate any change of DNA ploidy after Ad-p53 transfer. RESULTS: Ad-p53 transduced cells successfully expressed p53 and p21 proteins after 48 hours of Ad-p53 transduction. Synergistic growth inhibition by combination of Ad-p53 and cisplatin was detected only in SKOV3 and OVCAR-3 cells, but not in PA-1 cells. In p53 deleted SKOV3 cells, cisplatin treatment after Ad-p53 showed higher growth inhibition than the treatment before Ad-p53 transduction, and reverse relationship was observed in p53 mutated OVCAR-3 cells. In SKOV3 cells, the fraction of cells at G2/M phase increased after cisplatin treatment, however, it decreased dramatically with Ad-p53 transduction. CONCLUSION: The synergistic growth inhibition by combination of Ad-p53 and cisplatin may depend on the p53 status and the temporal sequence of cisplatin treatment, suggesting judicious selective application of this strategy in clinical trials.

In Vitro Uptakes of Radiolabeled IVDU and IVFRU in Herpes Simplex Virus Type-1 Thymidine Kinase (HSV1-tk) Gene Transduced Morris Hepatoma Cell Line / 대한핵의학회잡지

PURPOSE: The herpes simplex virus type 1 thymidine kinase gene (HSV1-tk) is an attractive candidate as a reporter gene in noninvasive reporter gene monitoring system. The HSV1-tk gene was chosen as a reporter gene, because it has been extensively studied, and there are appropriate reporter probes, substrates of HSV1-tk gene product, to apply for HSV1-tk gene imaging. We used radiolabeled 5-iodovinyl-2'-deoxyuridine (IVDU) and 5-Iodovinyl-2'-fluoro-2'-deoxyuridine (IVFRU) as reporter probes for HSV1-tk gene monitoring system. MATERIALS AND METHODS: We prepared HSV1-tk gene transduced Morris hepatoma cell line using retroviral vector, MOLTEN containing HSV1-tk gene. And we confirmed the HSV1-tk gene expression by Northern blotting and Western blotting. We compared in vitro uptakes of radioiodinated IVDU and IVFRU to monitor HSV1-tk gene expression in Morris hepatoma cell line (MCA) and HSV1-tk gene tranduced MCA (MCA-tk) cells until 480 minutes. We also performed correlation analysis between percentage of HSV1-tk gene tranduced MCA cell % (MCA-tk%) and uptakes of radiolabeled IVDU or IVFRU. RESULTS: MCA-tk cell expressed HSV1-tk mRNA and HSV1-TK protein. Two compounds showed minimal uptake in MCA, but increased uptake was observed in MCA-tk. IVDU showed 4-fold higher accumulation than IVFRU at 480 min in MCA-tk (p 0.96) with increasing MCA-tk%. CONCLUSION: The radiolabeld IVDU and IVFRU showed higher specific accumulation in retrovirally HSV1-tk gene transfected Morris hepatoma cell line. Both IVDU and IVFRU could be used as good substrates for evaluation of HSV1-tk gene expression.

Growth Suppression by Adenovirus-mediated Gene Transfer of p16/INK4a in Glioma Cell Lines

No abstract available.

Herpes Simplex virus thymidine kinase gene therapy delivered by retroviral or adenoviral vector in mouse model of lewis lung carcinoma / 결핵

BACKGROUND: The antitumor effects of herpes simplex virus thymidine kinase(HSV-tk) and ganciclovir(GCV) strategies for cancer gene therapy have a the following advantages:1) a direct cytotoxicity to HSV-tk modified cancer cells by GCV 2) a cell death by the local transfer of toxic metabolites from the HSV-tk modified cells to nearby unmodified tumor cells(bystander effect), and 3) in vivo bystander effect such as antitumor-immunity. Retroviral and adenoviral sequences can silence transgene expression in cells and mice. In this study, we investigated the above described advantages of HXV-tk/GCV strategy in Lewis lung cell and mouse lung cancer model using retroviral vector and adenoviral vector. Also, we observed whether the expression of a silenced gene can be reactivated by treating cell with butyrate. METHODS: Retrovirus-HSV-tk and adenovirus-HSV-tk vectors were used for the transduction of Lewis lung carcinoma(LLC) cells. The change of HSV-tk expression by butyrate was measured by Western blot.The antitumor activities containing bystander effect were observed in vivo(by MTT assay) and in vivo tumor models of various combinations of LLC and LLC-tk. RESULTS: 1. Butyrate induced the enhancement of HSV-tk expression from adenovirally transduced cells but not from retrovirally transduced cells. 2. Both retrovirus-HSV-tk and adenovirus-HSV-tk vectors with GCV treatment were effective for killing of tumor cell in vitro and suppression of LLC tumorigenicity. Bystander effect was responsible for killing of mixture of LLC-tk and LLC in vitro and in vivo-tumorigenicity model. CONCLUSION: Butyrate could augment adenoviral vector seems to be an effective approach for lung cancer therapy.

Adenovirus - Mediated gene Transfer of Wild - Type p53 Results in Restoration of Tumor - Suppressor Function in Glioma Cell Lines / 대한암학회지

PURPOSE: The replacement of functional genes into cells that lack genes or mutant genes is the basis of gene therapy. In cancer, where cells often have multiple genetic defects, the replacement of critical genes may suffice to suppress cell growth or induce cell death. In malignant brain tumors, p53 mutation are among the most frequently observed genetic findings and inactivation p53 suggests that p53 plays a critical role in carcinogenesis and tumor progression. Therefore, we study the successful transfer of the wild-type p53 gene using a replicative deficient adenovirus vector into human glioma and medulloblastoma c~ell lines. Meterials and Methods: The human glioma cell line T-98G, U-87MG, U-373MG were used. To determine the efficiency of the adenovirus vector, cell lines were transfected with the Ad-p gal and analysed with X-Gal staining. Cell viability was determined by trypan blue exclusion every day after infection and Westem blot analysis was used to conform the expression of the exogenous p53 protein. RESULTS: Cell growth of the Ad-CMV-p53 infected U-373MG, and U-87MG was significantly suppressed. It appeared that exogenous p53 protein expression had an earlier ad more profound suppressive effect on U-373MG having a mutated p53 gene than on U-87MG having a wild-type p53. The expression of the exogenous p53 was more than 10 times higher than the expression of the endogenous p53. To examine the decreased viability, U-373MG was stained with Hochest 33258 and detected nuclear condensation and apoptic body. Staining results suggest that cells undergo apoptosis. CONCLUSION: The replicative deficient adenoviral vector can transfer and express p53 in human glioma cell lines in vitro, restoring wild-type p53 tumor suppressor functions. The restoration of normal p53-encoded protein in the mutant ceil lines induced cell death. The high expression of the newly transduced protein had different effects on the growth rate of the infected cell lines depending on the p53 status of the cells.