Electron microscopic studies of replicating SV 40 DNA

Electron microscopic observation of replicating SV 40 DNA has revealed the existence of two types of RF, e form and (1 form. The frequency of RF at 54 hours after infection was 8.9% for the e form and 4.3% for the (1 form. Morphological evidence exhibits that in (1 form RF the tails are, predominantly, shorter than the viral genome and double length SV-40 genomes are also capable of replication in SV-40 infected VERO cells.</p

Circular DNA's from HeLa cell nuclei and mitochondria

An electron microscopic observation was made on the DNA's extracted from purified HeLa cell nuclei, mitochondria, and the whole cell, and fractionated by ethidium bromide-cesium chloride density gradient method or sucrose density gradient method. Nuclear DNA presents mainly long linear DNA derived from fragmented chromosomal DNA. In addition to this, the existence of small circular DNA molecules measuring 0.32 -1.78 &#956;, was confirmed. Mitochondrial DNA was mainly circular DNA, which measured 4.87 &#956; in the mean value of the contour lengths in the highest frequency group, and small circular DNA molecules, measuring 0.3-1.01 &#956; in contour length, were also found in an extremely low frequency.</p

Relationship between molecular length and biological activity of SV40 DNA

The correlation of infectivity to the length of SV 40 DNA by dilute and undiluted passage was described. DNA was extracted from purified virions by Marmur's method, and propagation of virus was done using VERO cells. The infectivity of SV 40 (simian virus 40) ran parallel with the length of its DNA. Undiluted passage caused shortening of DNA and decrease in infectivity, but when these undiluted group was passaged dilutely, length of DNA approached the original length and the infectivity recovered. In undiluted passage group small circular DNAs under 1.0,11_, so far not reported in the SV 40 DNA, were found in low frequency. Replicating form and dimers were also noted from virions and the nuclei of SV 40 infected VERO cells.</p

Usefulness of Thoracoscopic Debridement for Chronic Empyema after an Extrapleural Pneumonectomy

We present the case of a 65-year-old Japanese man diagnosed with chronic empyema (without a bronchopleural fistula) that occurred 7 months after he underwent an extrapleural pneumonectomy for right malignant pleural mesothelioma (MPM). Following thoracic drainage and irrigation for 1 month, we performed surgery by a thoracoscopic approach, in light of his general condition. We performed debridement and removal of the Gore-Tex polytetrafluoroethylene (PTFE) patch that had been used for the reconstruction of the diaphragm and the pericardium. The empyema had not relapsed when he died from recurrence of the MPM at 4 months after the thoracoscopic surgery. This patientʼs case suggests that thoracoscopic debridement and patch removal can be a therapeutic option for not only early-stage (exudative or fibrinopurulent) empyema but also late-stage (organized and chronic) empyema without a bronchopleural fistula, particularly for patients in poor general condition

Absence of scalenus anterior muscle.

A rare anomaly of the scalenus muscles is described. In this case, the right scalenus anterior muscle was absent. As a substitute for this muscle, some aberrant muscle slips arose from the lower vertebrae and descended in front of the ventral rami of the lower cervical nerves. These aberrant slips then ran between the ventral rami of the the eighth cervical and first thoracic nerves, and were fused with the right scalenus medius muscle. Thus, the subclavian artery and vein ran in front of the aberrant slips, together with the ventral ramus of the first thoracic nerve. The aberrant muscle slips issued 2 accessory bundles. One bundle ran between the ventral rami of the fourth and fifth cervical nerves and was fused with the scalenus medius muscle; the other bundle ran between the ventral rami of the fifth and sixth cervical nerves and was fused with the scalenus medius muscle.</p

Drug Resistance to EGFR Tyrosine Kinase Inhibitors for Non-small Cell Lung Cancer

Non-small cell lung cancer (NSCLC) harboring an activating mutation within the epidermal growth factor receptor (EGFR) was defined as a clinically distinct molecular group. These lesions show oncogene addiction to EGFR and dramatic responses to the EGFR tyrosine kinase inhibitors (TKIs). Several large Phase III trials have shown that EGFR-TKIs improved the progression-free survival of patients with EGFR mutant NSCLC compared to conventional chemotherapy. However, the long-term effectiveness of EGFR-TKIs is usually limited because of acquired drug resistance. To overcome this resistance to EGFR-TKIs, it will be essential to identify the specific mechanisms underlying the resistance. Many investigators have attempted to identify the mechanisms using preclinical models and drug-resistant clinical samples. As a result, several mechanisms have been showed to be responsible for the resistance, but not all of the relevant mechanisms have been uncovered. In this review, we provide an overview of mechanisms underlying drug-resistance to EGFR-TKIs, focusing on results obtained with preclinical models, and we present some possible strategies to overcome the EGFR-TKI resistance

Quantitative laser diffraction method for the assessment of protein subvisible particles

Shinichiro Totoki, Gaku Yamamoto, Kouhei Tsumoto, Susumu Uchiyama, Kiichi Fukui. Quantitative Laser Diffraction Method for the Assessment of Protein Subvisible Particles. Journal of Pharmaceutical Sciences, Volume 104, Issue 2, 2015, Pages 618-626. https://doi.org/10.1002/jps.24288

Reconstruction of Anterior Chest Wall with Polypropylene Mesh: Two Primary Sternal Chondrosarcoma Cases

　Primary sternal chondrosarcoma is a rare malignant tumor that is refractory to chemotherapy and radiation. Effective therapy is radical resection of the tumor. We present two patients with primary sternal chondrosarcoma who underwent a radical resection of the lower half of the sternum and bilateral ribs, followed by reconstruction with 2 sheets of polypropylene mesh layered orthogonally. The patients have maintained almost the same pulmonary function as preoperative values, with stability of the chest wall. Although there are various ways to reconstruct the anterior chest wall, reconstruction with polypropylene mesh layered orthogonally is an easy-to-use and sufficient method

Transient receptor potential channels in Alzheimer's disease

AbstractCognitive impairment and emotional disturbances in Alzheimer's disease (AD) result from the degeneration of synapses and neuronal death in the limbic system and associated regions of the cerebral cortex. An alteration in the proteolytic processing of the amyloid precursor protein (APP) results in increased production and accumulation of amyloid β-peptide (Aβ) in the brain. Aβ can render neurons vulnerable to excitotoxicity and apoptosis by disruption of cellular Ca2+ homeostasis and neurotoxic factors including reactive oxygen species (ROS), nitric oxide (NO), and cytokines. Many lines of evidence have suggested that transient receptor potential (TRP) channels consisting of six main subfamilies termed the TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPP (polycystin), TRPML (mucolipin), and TRPA (ankyrin) are involved in Ca2+ homeostasis disruption. Thus, emerging evidence of the pathophysiological role of TRP channels has yielded promising candidates for molecular entities mediating Ca2+ homeostasis disruption in AD. In this review, we focus on the TRP channels in AD and highlight some TRP “suspects” for which a role in AD can be anticipated. An understanding of the involvement of TRP channels in AD may lead to the development of new target therapies

Silenced Expression of NFKBIA in Lung Adenocarcinoma Patients with a Never-smoking History

Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas. We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. NFKBIA expression was evaluated using immunohistochemistry. NFKBIA expression was negative in 16 of the 101 samples (15.8%). EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. Negative NFKBIA expression was observed significantly more frequently among the tumors with none of the three genetic alterations compared to those with such alterations (p＝0.009). In addition, negative NFKBIA expression was significantly more frequent among the EGFR-wild type samples compared to the EGFR-mutant samples (p＝0.013). In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion