Dorsal and Volar Approaches for Proximal Interphalangeal Joint Replacement: Comparing Outcomes Through Systematic Review and Meta-Analysis.

Background: The 2 primary surgical approaches for proximal interphalangeal joint (PIPJ) arthroplasty, dorsal or volar, have been extensively described in the literature. However, the ongoing debate regarding which approach offers superior results or is associated with fewer complications persists. This systematic review aims to compare the outcomes of PIPJ arthroplasty between the dorsal and volar approaches.

A novel case of simultaneous tracheal stenting and endobronchial valve (EBV) deployment for tracheal stenosis and persistent air leak guided by an endobronchial collateral ventilation assessment system and digital chest drain in malignant esophageal carcinoma.

Persistent air leak may complicate malignant disease of the thorax, causing significant morbidity and mortality. A 51-year-old male with a 30-pack-year history of smoking was diagnosed with metastatic esophageal carcinoma with invasion into the right upper lobe of the lung. He developed a large right hydropneumothorax complicated by empyema leading to persistent air leak despite the insertion of two chest drains.

Pleuroparenchymal sarcoidosis: A rare manifestation mimicking metastatic lung cancer.

A 66-year-old male from Myanmar presented with 3 months of cough and constitutional symptoms. He was an ex-tobacco user with no significant medical or exposure history. Chest x-ray showed ill-defined bilateral opacities and a left pleural effusion.

Impact of Smoking and Brain Metastasis on Outcomes of Advanced EGFR Mutation Lung Adenocarcinoma Patients Treated with First Line Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors.

Objectives: This purpose of this study was to examine clinical-pathologic factors--particularly smoking and brain metastases--in EGFR mutation positive (M(+)) lung adenocarcinoma (ADC) to determine their impact on survival in patients treated with first line EGFR TKI.

Methods: A retrospective review of EGFR mutation reflex testing experience for all ADC diagnosed at a tertiary Asian cancer centre from January 2009 to April 2013. Amongst this cohort, patients with advanced EGFR M(+) ADC treated with first line EGFR TKI were identified to determine factors that influence progression free and overall survival.

Metabolic regulation of Drosophila apoptosis through inhibitory phosphorylation of Dronc.

Apoptosis ensures tissue homeostasis in response to developmental cues or cellular damage. Recently reported genome-wide RNAi screens have suggested that several metabolic regulators can modulate caspase activation in Drosophila. Here, we establish a previously unrecognized link between metabolism and Drosophila apoptosis by showing that cellular NADPH levels modulate the initiator caspase Dronc through its phosphorylation at S130.

Metabolic control of oocyte apoptosis mediated by 14-3-3zeta-regulated dephosphorylation of caspase-2.

Xenopus oocyte death is partly controlled by the apoptotic initiator caspase-2 (C2). We reported previously that oocyte nutrient depletion activates C2 upstream of mitochondrial cytochrome c release. Conversely, nutrient-replete oocytes inhibit C2 via S135 phosphorylation catalyzed by calcium/calmodulin-dependent protein kinase II.

Mitochondrial localization of Reaper to promote inhibitors of apoptosis protein degradation conferred by GH3 domain-lipid interactions.

Morphological hallmarks of apoptosis result from activation of the caspase family of cysteine proteases, which are opposed by a pro-survival family of inhibitors of apoptosis proteins (IAPs). In Drosophila, disruption of IAP function by Reaper, HID, and Grim (RHG) proteins is sufficient to induce cell death. RHG proteins have been reported to localize to mitochondria, which, in the case of both Reaper and Grim proteins, is mediated by an amphipathic helical domain known as the GH3.

HLA-B-associated transcript 3 (Bat3)/Scythe is essential for p300-mediated acetylation of p53.

In response to DNA damage, p53 undergoes post-translational modifications (including acetylation) that are critical for its transcriptional activity. However, the mechanism by which p53 acetylation is regulated is still unclear. Here, we describe an essential role for HLA-B-associated transcript 3 (Bat3)/Scythe in controlling the acetylation of p53 required for DNA damage responses.

Direct ribosomal binding by a cellular inhibitor of translation.

During apoptosis and under conditions of cellular stress, several signaling pathways promote inhibition of cap-dependent translation while allowing continued translation of specific messenger RNAs encoding regulatory and stress-response proteins. We report here that the apoptotic regulator Reaper inhibits protein synthesis by binding directly to the 40S ribosomal subunit. This interaction does not affect either ribosomal association of initiation factors or formation of 43S or 48S complexes.

A GH3-like domain in reaper is required for mitochondrial localization and induction of IAP degradation.

Reaper is a potent pro-apoptotic protein originally identified in a screen for Drosophila mutants defective in apoptotic induction. Multiple functions have been ascribed to this protein, including inhibition of IAPs (inhibitors of apoptosis); induction of IAP degradation; inhibition of protein translation; and when expressed in vertebrate cells, induction of mitochondrial cytochrome c release. Structure/function analysis of Reaper has identified an extreme N-terminal motif that appears to be sufficient for inhibition of IAP function.

The microtubule-destabilizing kinesin XKCM1 is required for chromosome positioning during spindle assembly.

Xenopus kinesin catastrophe modulator-1 (XKCM1) is a Kin I kinesin family member that uses the energy of ATP hydrolysis to depolymerize microtubules. We demonstrated previously that XKCM1 is essential for mitotic-spindle assembly in vitro and acts by regulating microtubule dynamics as a pure protein, in extracts and in cells. A portion of the XKCM1 pool is specifically localized to centromeres during mitosis and may be important in chromosome movement.

XKCM1 acts on a single protofilament and requires the C terminus of tubulin.

The stability of microtubules during the cell-cycle is regulated by a number of cellular factors, some of which stabilize microtubules and others that promote breakdown. XKCM1 is a kinesin-like protein that induces microtubule depolymerization and is required for mitotic spindle assembly. We have examined the binding and depolymerization effects of XKCM1 on different tubulin polymers in order to learn about its mechanism of action.