A left thoracic approach in a prone position for thoracoscopic thoracic duct ligation in a patient with post-esophagectomy chylothorax: A case report

INTRODUCTION: We debate whether or not to approach from right thorax for the left chylothorax afteresophagectomy.PRESENTATION OF CASE: A 50 s-year-old female underwent right-sided thoracoscopic esophagectomywith three-field lymphadenectomy for esophageal carcinoma (type 0-IIa, 3.4 × 2.2 cm, T1bN0M0, StageIA), followed by reconstruction with esophagogastric anastomosis through the posterior mediastinum.The thoracic duct was excised and ligated. The left thoracic drainage increased to 2115 mL/day on thefifth postoperative day. Thoracic duct injury was diagnosed, and surgery was performed on sixth post-operative day. With the patient in a prone position, the thoracic duct was ligated successfully underthoracoscopy in the left thorax. The leakage point was found in the crushed duct by 8.8-mm tita-nium clips. Then, we performed mass ligation of the thoracic duct with 11-mm titanium clips belowthe leakage point after careful dissection. The surgery took 58 min, with an estimated total blood lossof 0 g.DISCUSSION: Although thoracic duct is anatomically located on the right side of the descending aorta,we employed a left-sided thoracoscopic approach due to the chylous leakage in the left thorax. With thepatient in the prone position, surgeons can easily convert from a left thoracic approach to a right thoracicapproach immediately without postural change if the thoracic duct cannot be found in the left thoraciccavity.CONCLUSION: This technique is useful and should be considered for patients with left chylothorax

In Silico Identification of Short Nucleotide Sequences Associated with Gene Expression of Pollen Development in Rice

Microarray analysis of tiny amounts of RNA extracted from plant section samples prepared by laser microdissection (LM) can provide high-quality information on gene expression in specified plant cells at various stages of development. Having joined the LM-microarray analysis project, we utilized such genome-wide gene expression data from developing rice pollen cells to identify candidates for cis-regulatory elements for specific gene expression in these cells. We first found a few clusters of gene expression patterns based on the data from LM-microarrays. On one gene cluster in which the members were specifically expressed at the bicellular and mature pollen mitotic stages, we identified gene cluster fingerprints (GCFs), each of which consists of a short nucleotide representing the gene cluster. We expected that these GCFs would contain cis-regulatory elements for stage- and tissue-specific gene expression, and we further identified groups of GCFs with common core sequences. Some criteria, such as frequency of occurrence in the gene cluster in contrast to the total tested gene set, flanking sequence preference and distribution of combined GCF sets in the gene regions, allowed us to limit candidates for cis-regulatory sequences for specific gene expression in rice pollen cells to at least 20 sets of combined GCFs. This approach should provide a general purpose algorithm for identifying short nucleotides associated with specific gene expression

In Vivo Mitochondrial p53 Translocation Triggers a Rapid First Wave of Cell Death in Response to DNA Damage That Can Precede p53 Target Gene Activation

p53 promotes apoptosis in response to death stimuli by transactivation of target genes and by transcription-independent mechanisms. We recently showed that wild-type p53 rapidly translocates to mitochondria in response to multiple death stimuli in cultured cells. Mitochondrial p53 physically interacts with antiapoptotic Bcl proteins, induces Bak oligomerization, permeabilizes mitochondrial membranes, and rapidly induces cytochrome c release. Here we characterize the mitochondrial p53 response in vivo. Mice were subjected to γ irradiation or intravenous etoposide administration, followed by cell fractionation and immunofluorescence studies of various organs. Mitochondrial p53 accumulation occurred in radiosensitive organs like thymus, spleen, testis, and brain but not in liver and kidney. Of note, mitochondrial p53 translocation was rapid (detectable at 30 min in thymus and spleen) and triggered an early wave of marked caspase 3 activation and apoptosis. This caspase 3-mediated apoptosis was entirely p53 dependent, as shown by p53 null mice, and preceded p53 target gene activation. The transcriptional p53 program had a longer lag phase than the rapid mitochondrial p53 program. In thymus, the earliest apoptotic target gene products PUMA, Noxa, and Bax appeared at 2, 4, and 8 h, respectively, while Bid, Killer/DR5, and p53DinP1 remained uninduced even after 20 h. Target gene induction then led to further increase in active caspase 3. Similar biphasic kinetics was seen in cultured human cells. Our results suggest that in sensitive organs mitochondrial p53 accumulation in vivo occurs soon after a death stimulus, triggering a rapid first wave of apoptosis that is transcription independent and may precede a second slower wave that is transcription dependent

p53 Has a Direct Apoptogenic Role at the Mitochondria

p53 induces apoptosis by target gene regulation and transcription-independent signaling. However, a mechanism for the latter was unknown. We recently reported that a fraction of induced p53 translocates to the mitochondria of apoptosing tumor cells. Targeting p53 to mitochondria is sufficient to launch apoptosis. Here, we provide evidence that p53 translocation to the mitochondria occurs in vivo in irradiated thymocytes. Further, we show that the p53 protein can directly induce permeabilization of the outer mitochondrial membrane by forming complexes with the protective BclXL and Bcl2 proteins, resulting in cytochrome c release. p53 binds to BclXL via its DNA binding domain. We probe the significance of mitochondrial p53 and show that tumor-derived transactivation-deficient mutants of p53 concomitantly lose the ability to interact with BclXL and promote cytochrome c release. This opens the possibility that mutations might represent “double-hits” by abrogating the transcriptional and mitochondrial apoptotic activity of p53