Currently 18 monoclonal antibodies were approved by FDA for inj ection into humans for therapeutic or diagnostic purpose. And 146 clinical trials are under way to evaluate the efficacy of monoclonal antibodies as anti-cancer agents, which comprise 9% of clinical trials in cancer therapy field. When considering a lot of disappointment and worries existed in this field during the past 15 years, this boom could be called as resurrection. Antibodies have several merits over small molecule drug. First of all it is easier and faster in development, as proper immunization of the target proteins usually raises good antibody response. The side effect s of antibodies are more likely to be checked out in immunohistomchemical staining of whole human tissues. Antibody has better pharmacokinetics, which means a longer half-life. And it is non-toxic as it is purely a natural drug. Vast array of methods was developed to get the recombinant antibodies to be used as drug. The mice with human immunoglobulin genes were generated. Fully human antibodies can be developed in fast and easy way from these mice through immunization. These mice could make even human monoclonal antibodies against any human antigen like albumin. The concept of combinatorial library was also actively adopted for this purpose. Specific antibodies can be screened out from phage, mRNA, ribosomal library displaying recombinant antibodies like single chain Fvs or Fabs. Then the coding genes of these specific antibodies are obtained from the selected protein-gene units, and used for industrial scale production. Both naive and immunized libraries are proved to be effective for this purpose. In post-map arena, antibodies are receiving another spotlight as molecular probes against numerous targets screened out from functional genomics or proteomics. Actually many of these antibodies used for this purpose are already human ones. Through alliance of these two actively growing research areas, antibody would play a central role in target discovery and drug development.
Animals ; Antibodies ; Antibodies, Monoclonal ; Antibody Formation ; Bacteriophages ; Clinical Coding ; Genes, Immunoglobulin ; Genomics ; Half-Life ; Humans ; Immunization ; Mice ; Molecular Probes ; Pharmacokinetics ; Proteomics ; RNA, Messenger ; Single-Chain Antibodies

No abstract available.
Antibodies*

All solid tumors require the induction of new blood vessel to grow. The neovascularization of tumor tissue(angiogenesis) is considered essential for tumor growth, proliferation and eventually metastasis. Recent reports have demonstrated that the intensity of tumor angiogenesis in prostate and other tumors may be of prognostic value. We analyzed the prognostic significance of microvessel quantitation in bladder carcinoma. Microvessels were identified by immunohistochemistry using antibodies to endothelial marker, factor VIII-related antigen. The three most vascular area within a tumor were selected, and the microvessels within a x200 microscopic field of each area were counted by an investigator. The significant relationship was observed between microvessel counts and recurrence rate in 17 patients with superficial bladder cancer. Microvessel counts correlated with stage, grade, lymph node and distant metastasis, and 2 year disease free survival rate in 28 patients with invasive bladder cancer. In 15 patients with invasive cancer who were not showed distant metastasis, tumors from patients who experienced distant metastasis had higher microvessel counts than did tumors from patients who were disease- free(75.7118.59 and 61.7517.78), these values were not significantly different(p=0.081). These findings suggest that assessment of angiogenesis by microvessel quantitation may be a valuable method to predict metastatic potential of tumors, survival and the candidates for adjuvant therapy in patients with invasive bladder cancer.
Antibodies ; Blood Vessels ; Disease-Free Survival ; Humans ; Immunohistochemistry ; Lymph Nodes ; Microvessels ; Neoplasm Metastasis ; Prostate ; Recurrence ; Research Personnel ; Urinary Bladder Neoplasms* ; Urinary Bladder* ; von Willebrand Factor

No abstract available.
Brain Stem* ; Cysticercus* ; Granuloma*

PURPOSE: Retrospective study was done to evaluate the causes of priapism lasting for over 24 hours induced by intracavernous vasoactive agents. MATERIALS AND METHODS: Thirteen patients of priapism lasting for 24-60 hours, induced by intracavernous vasoactive drugs, were retrospectively evaluated using medical records or by telephone interviews. Injected vasoactive drugs, providers of the drugs, purpose of the injection, reasons leaving the priapism untreated so long, treatment modalities of the priapism, and change of potency after the treatment were evaluated. RESULTS: Only 2 patients (15.4%) were self-injected to treat erectile dysfunction by doctor's prescription. The others, who received the drugs without doctor's prescription, had injections to enhance their potency (46.1%, n=6) or to treat premature ejaculation (15.4%, n=2). The drugs injected were papaverine (23.1%, n=3), papaverine and phentolamine (23.1%, n=3) or prostaglandin E1(7.7%, n=1), but unknown in 6 (46.1%). The reasons of leaving the priapism untreated were mostly due to lack of no knowledge about the priapism (53.8%, n=7). Aspiration and irrigation with alpha-agonist of corpus cavernosum were applied to all patients. Four patients who did not respond to the treatment underwent shunt operations. All the patients complained of weakened potency after the priapism. CONCLUSIONS: Priapism lasting for over 24 hours induced by intracavernous vasoactive drugs were mostly due to abuse or misuse of the drugs and resulted in weakened potency. To avoid this disaster, the drugs should be given to patients by doctor's prescription with full explanation about the side effects of the drug.
Disasters ; Erectile Dysfunction ; Humans ; Interviews as Topic ; Male ; Medical Records ; Papaverine ; Phentolamine ; Premature Ejaculation ; Prescriptions ; Priapism* ; Retrospective Studies

We had a case of respiratory difficulty following tracheal extubation due to bilateral vocal cord paralysis. The patient was a 66-year-old woman undergoing craniotomy for cerebellopontine angle meningioma. Anesthesia was uneventful. Spontaneous respiration resumed after reversal of neuromuscular blockade. Following extubation she showed inspiratory stridor, tachypnea, and chest retraction. Reintubation was done and then tracheostomy was performed. Every factor contributing vocal cord paralysis such as pressure on the nerve by an overexpanded endotracheal tube cuff, unique posture of the neck during the operation, and female gender, long operating time(about 11 hours) were seemed to be possible causes and we considered the interaction of these combinations responsible for the bilateral vocal cord paralysis. Eight weeks later, the patient's vocal cord function had returned to normal.
Aged ; Airway Extubation* ; Anesthesia ; Cerebellopontine Angle ; Craniotomy ; Female ; Humans ; Meningioma ; Neck ; Neuromuscular Blockade ; Posture ; Respiration ; Respiratory Sounds ; Tachypnea ; Thorax ; Tracheostomy ; Vocal Cord Paralysis* ; Vocal Cords*

No abstract available.
Brain* ; Krukenberg Tumor* ; Neoplasm Metastasis*

The author has examined the effect of cortical spreading depression(CSD) on the changes in extracellular concetration of aspartate and glutamate in the neocortex of anesthetized rats using microdialysis and high performance liquid chromatography(HPLC). The rats were prepared by halothane anesthesia and artificial ventilation. Rats were placed in a stereotaxic frame, and craniotomies were performed over the frontal and parietal cortexes on one side. The CSD was elicited by local application of KCI-soaked small pellets to the frontal cortex. The CSD was monitored by the changes of direct current(DC) potential in the parietal cortex. The microdialysis probe was implanted in the anterior part of the parietal cortex. Amino acids were analyzed by HPLC and fluorescence detection. Baseline concentration of the aspartate was 34.9+/-15.9nM and that of glutamate was 189.8+/-29.1nM(mean standard deviation). The perfusate for analysis was obtained 30 minutes after the beginning of the 300mM KCl induced CSD. Aspartate was found to increase to 146+/-55% baseline, glutamate up to 173+/-30% baseline(mean standard deviation). The increment of glutamate was statistically significant(p<0.05). Then 2M KCI-doaked pellets were applied for more frequent CSD amd the samples were collected. Aspartate increased up to 258+/-97% baseline, glutamate up to 174+/-57% baseline(mean standard deviation), The increment of glutamate and aspartate accompanying 2M KCI induced CSD were also statistically significant(p<0.05). These data suggest that the excitatory amino acids were released during the CSD and this may explain the various aspects of CSD that could contribute to the secondary neuronal damage in the compromised nerve cell.
Amino Acids ; Anesthesia ; Animals ; Aspartic Acid* ; Cerebral Cortex* ; Chromatography, High Pressure Liquid ; Cortical Spreading Depression* ; Craniotomy ; Excitatory Amino Acids ; Fluorescence ; Glutamic Acid* ; Halothane ; Microdialysis ; Neocortex ; Neurons ; Rabeprazole ; Rats* ; Ventilation

The author has performed an experimental study in order to investigate the effect of nimodipine on the production of CSF in 12 cats. The cats were divided into 2 groups, one for nimodipine intravenous infusion and the other for its vehicle infusion group. Using ventriculo-cisternal perfusion method, nimodipine and its vehicle were examined for their effects on CSF formation rate respectively. Baseline CSF formation rate was 22.5+/-2.9 microliter/min(S.E.) and it gradually reduced to 17.0+/-3.4 microliter/min(S.E.) after final infusion of nimodipine at 60 microgram/kg/min. Vehicle infusion revealed no significant change in CSF formation rate. Although the nimodipine insuion revealed declining tendency in CSF formation rate along with increment of nimodipine concentration, it was not statistically different from that of vehicle infusion group. Systolic blood pressure was significantly reduced after nimodipine infusion(133+/-31.8mmHg at baseline, 93.9+/-19.1mmHg at the end of the experiment) on oneway ANOVA test and it was significantly different from that in vehicle infusion group(p<0.01).
Animals ; Blood Pressure ; Cats ; Infusions, Intravenous ; Nimodipine* ; Perfusion

No abstract available.
Stroke*