A-MPDU aggregation with optimal number of MPDUs for delay requirements in IEEE 802.11ac.

In this paper, we propose a method that estimates an average delay of frames for each queue and finds an optimal number of aggregated Medium Access Control (MAC) Protocol Data Units (MPDUs) to maximize the system throughput with satisfying the delay requirement of each queue when using the Aggregate MPDU (A-MPDU) aggregation in IEEE 802.11ac. The delay is defined as the sum of the queuing delay and the service delay. If few frames in a queue are aggregated, the frames which remain in the queue for next transmissions may violate the target delay because of the overhead for the next transmissions such as the backoff time, Physical Layer Convergence Procedure (PLCP) preamble, and PLCP header. If many of the frames in the queue are aggregated, the frames of the queue and the other queues may violate their target delays because of a long transmission duration and a long channel occupancy. In this paper, we obtain the average delay for each queue and the optimal number of aggregated MPDUs for the delay requirement of each queue in IEEE 802.11ac. At the last, we evaluate and show the performance of our proposed method through simulations. The simulation results show that the proposed method can estimate the average delay for each queue accurately. The simulation results also show that the proposed method can obtain the violation rates on the target delays less than 0.1. Furthermore, the simulation results show that the proposed method can yield higher system throughput than other conventional methods.

Cerebral-perfusion-based single-photon emission computed tomography (SPECT) staging using NeuroGam® in patients with moyamoya disease.

BACKGROUND AND PURPOSE: Cerebral angiography (CA) is the gold standard for moyamoya disease (MMD) staging and diagnosis, but CA findings are not well correlated with clinical symptoms. The purpose of this study was to establish novel cerebral-perfusion-based staging for MMD that is well correlated with clinical symptoms. MATERIALS AND METHODS: From 2010 to 2015, regional cerebrovascular reserve (rCVR) was examined by single-photon emission computed tomography (SPECT) using NeuroGam® (Segamicorp, Houston, TX, USA) in 30 patients (17 women, 13 men; 60 hemispheres; mean 42.0 years old [range 5-60 years old]) with MMD, which was diagnosed by CA and magnetic resonance angiography (MRA). Brain CT or brain magnetic resonance imaging (MRI) was used to evaluate neurological conditions such as transient ischemic attack (TIA), cerebral hemorrhage, and cerebral infarction. A novel staging system for MMD was developed by combining findings from CA, MRI, and SPECT with NeuroGam®. RESULTS: Our novel staging system was strongly associated with clinical symptoms. Twenty-two hemispheres out of 60 were categorized as stage I, 24 hemispheres were categorized as stage II, and 14 hemispheres were categorized as stage III. Hemispheres with higher scores exhibited a higher incidence of clinical symptoms. These findings indicate that cerebral-perfusion-based staging is predictive of MMD clinical symptoms. CONCLUSION: Perfusion-based SPECT staging correlates well with clinical symptoms and may be a reliable alternative to the Suzuki staging by CA.

Inhibitory effect of snake venom toxin on NF-κB activity prevents human cervical cancer cell growth via increase of death receptor 3 and 5 expression.

We previously found that snake venom toxin inhibits nuclear factor kappa B (NF-κB) activity in several cancer cells. NF-κB is implicated in cancer cell growth and chemoresistance. In our present study, we investigated whether snake venom toxin (SVT) inhibits NF-κB, thereby preventing human cervical cancer cell growth (Ca Ski and C33A). SVT (0-12 µg/ml) inhibited the growth of cervical cancer cells by the induction of apoptotic cell death. These inhibitory effects were associated with the inhibition of NF-κB activity. However, SVT dose dependently increased the expression of death receptors (DRs): DR3, DR5 and DR downstream pro-apoptotic proteins. Exploration of NF-κB inhibitor (Phenylarsine oxide, 0.1 µM) synergistically further increased SVT-induced DR3 and DR5 expressions accompanied with further inhibition of cancer cells growth. Moreover, deletion of DR3 and DR5 by small interfering RNA significantly abolished SVT-induced cell growth inhibitory effects, as well as NF-κB inactivation. Using TNF-related apoptosis-inducing ligand resistance cancer cells (A549 and MCF-7), we also found that SVT enhanced the susceptibility of chemoresistance of these cancer cells through down-regulation of NF-κB, but up-regulation of DR3 and DR5. In vivo study also showed that SVT (0.5 and 1 mg/kg) inhibited tumor growth accompanied with inactivation of NF-κB. Thus, our present study indicates that SVT could be applicable as an anticancer agent for cervical cancer, or as an adjuvant agent for chemoresistant cancer cells.

Anti-cancer effect of snake venom toxin through down regulation of AP-1 mediated PRDX6 expression.

Snake venom toxin (SVT) from Vipera lebetina turanica contains a mixture of different enzymes and proteins. Peroxiredoxin 6 (PRDX6) is known to be a stimulator of lung cancer cell growth. PRDX6 is a member of peroxidases, and has calcium-independent phospholipase A2 (iPLA2) activities. PRDX6 has an AP-1 binding site in its promoter region of the gene. Since AP-1 is implicated in tumor growth and PRDX6 expression, in the present study, we investigated whether SVT inhibits PRDX6, thereby preventing human lung cancer cell growth (A549 and NCI-H460) through inactivation of AP-1. A docking model study and pull down assay showed that SVT completely fits on the basic leucine zipper (bZIP) region of c-Fos of AP-1. SVT (0-10 µg/ml) inhibited lung cancer cell growth in a concentration dependent manner through induction of apoptotic cell death accompanied by induction of cleaved caspase-3, -8, -9, Bax, p21 and p53, but decreased cIAP and Bcl2 expression via inactivation of AP-1. In an xenograft in vivo model, SVT (0.5 mg/kg and 1 mg/kg) also inhibited tumor growth accompanied with the reduction of PRDX6 expression, but increased expression of proapoptotic proteins. These data indicate that SVT inhibits tumor growth via inhibition of PRDX6 activity through interaction with its transcription factor AP-1.

A solitary large radioiodine accumulative lung lesion in high-dose 131i therapeutic scan: bronchial atresia with mucocele.

We reported a large radioiodine accumulative lung lesion on I therapeutic whole-body scan performed in a 50-year-old woman for thyroid cancer ablation therapy. Previously, her chest radiography and contrast-enhanced chest CT images showed bronchial atresia in the left upper lobar bronchus and mucus-filled dilated distal bronchus. Bronchial mucocele was confirmed by CT-guided percutaneous transthoracic needle aspiration. Bronchial atresia is a rare congenital abnormality associated with the mucocele.

Role of ¹8F-FDG PET/CT in differentiation of a benign lesion and metastasis on the ribs of cancer patients.

OBJECTIVE: Incidental 18-Fluoro-2-deoxyglucose positron emission tomography ((18)F-FDG) uptake in the ribs is a relatively common finding on positron emission tomography/computed tomography (PET/CT) images of cancer patients. This study examined the role of (18)F-FDG PET/CT in differentiating between benign lesions and metastases on the ribs. METHODS: This study included 264 lesions in 172 PET/CT cases with underlying malignancy showing newly developed indeterminate (18)F-FDG rib uptake between June 2009 and May 2010. Patients with more than five FDG rib uptakes or hematologic malignancy were excluded. Malignancy was confirmed either histologically or by imaging studies, and clinical follow-up with serial images was at least 6 months. The maximum standardized uptake value (SUV(max)) of the rib lesion was recorded. The FDG uptake patterns (focal or segmental; discrete or non-discrete) and CT findings (evidence of fracture, soft tissue lesions, osteoblastic and/or osteolytic lesions) were recorded. RESULTS: There were 206 benign lesions and 58 metastases. The SUV(max) was significantly higher in the metastatic group (3.0 ± 1.8) than in the benign group (2.5 ± 1.1), (P=.014). For the differential diagnosis between benign and metastatic lesions, the best SUV(max) cut-off was determined to be 2.4. Significant indicators for metastasis were a segmental FDG uptake pattern (OR=10.262, 95% CI 4.151-25.371), presence of an osteoblastic/-lytic lesion (OR=22.903, 95% CI 10.468 to 50.108) and the absence of fractures on CT (OR=291.629, 95% CI 39.09-2175.666). CONCLUSION: SUV(max) alone is not sufficient to differentiate benign and metastatic rib lesions in cancer patients. The diagnostic accuracy can be further increased when findings of the CT part of PET/CT are considered.