Eliminating the Performance Anomaly of 802.11b

Abstract. In this paper, we propose a mechanism to eliminate the per-formance anomaly of IEEE 802.11b. Performance anomaly happens when nodes that have different transmission rates are in the same wireless cell. All the nodes in the cell might experience the same throughput even though their transmission rates are different because DCF of WLAN provides equal probability of channel access, but it does not guarantee the equal utilization of the wireless channel among the nodes. To reduce such a performance anomaly, we adjust the frame size proportionally depending on the bit rate. Additionally, our scheme eliminates the per-formance anomaly in multi-hop case. Simulation study shows that our scheme achieves an improvement in the aggregate throughput and the fairness.

Susceptibility to Oxidative Stress is Greater in Korean Patients with Coronary Artery Disease than Healthy Subjects

There are some evidences that the increased oxidative stress and thus increased oxidizability of lipoproteins and DNA can contribute to the development of certain human diseases, such as cardiovascular disease. To confirm the association of DNA damage with cardiovascular disease, we investigated susceptibility of DNA to oxidation in lymphocytes and oxidative stress related parameters in blood of patients with coronary artery disease (CAD). Subjects were consisted of 42 patients (27 men, 15 women) with documented CAD and 49 apparently healthy subjects (33 men, 16 women) as controls. Cellular DNA damage induced by 100 µM H2O2 was measured using Comet assay and quantified by TL. There were no differences in age (61.4 ± 1.7 years vs 62.0 ± 2.2 years) between the two groups. All the findings were shown to be independent of either sex or smoking habit. The patients showed significantly higher TL (87.3 ± 1.6 µm) compared to the control (79.3 ± 1.7 µm, p<0.01). Plasma TRAP, vitamin C, γ-tocopherol, and α-carotene levels in patients group were lower than those of control groups, while erythrocytic catalase activity increased in patients group. In conclusion, we observed that reduced overall antioxidant status was closely connected to higher susceptibility of DNA damage in CAD patients

The Effect of Dexmedetomidine on the Mini-Cog Score and High-Mobility Group Box 1 Levels in Elderly Patients with Postoperative Neurocognitive Disorders Undergoing Orthopedic Surgery

Dexmedetomidine prevents postoperative cognitive dysfunction by inhibiting high-mobility group box 1 (HMGB1), which acts as an inflammatory marker. This study investigated the HMGB1 levels and the cognitive function using a Mini-Cog© score in elderly patients undergoing orthopedic surgery with dexmedetomidine infusion. In total, 128 patients aged ≥ 65 years were analyzed. The patients received saline in the control group and dexmedetomidine in the dexmedetomidine group until the end of surgery. Blood sampling and the Mini-Cog© test were performed before the surgery and on postoperative days 1 and 3. The primary outcomes were the effect of dexmedetomidine on the HMGB1 levels and the Mini-Cog© score in terms of postoperative cognitive function. The Mini-Cog© score over time differed significantly between the groups (p = 0.008), with an increase in the dexmedetomidine group. The postoperative HMGB1 levels increased over time in both groups; however, there was no significant difference between the groups (p = 0.969). The probability of perioperative neurocognitive disorders decreased by 0.48 times as the Mini-Cog© score on postoperative day 3 increased by 1 point. Intraoperative dexmedetomidine has shown an increase in the postoperative Mini-Cog© score. Thus, the Mini-Cog© score is a potential tool for evaluating cognitive function in elderly patients

Chronic intermittent form of isovaleric aciduria in a 2-year-old boy

Isovaleric aciduria (IVA) is caused by an autosomal recessive deficiency of isovaleryl-CoA dehydrogenase (IVD). IVA presents either in the neonatal period as an acute episode of fulminant metabolic acidosis, which may lead to coma or death, or later as a "chronic intermittent form" that is associated with developmental delays, with or without recurrent acidotic episodes during periods of stress, such as infections. Here, we report the case of a 2-year old boy with IVA who presented with the chronic intermittent form. He was admitted to Asan Medical Center Children's Hospital with recurrent vomiting. Metabolic acidosis, hyperammonemia, elevated serum lactate and isovalerylcarnitine levels, and markedly increased urine isovalerylglycine concentration were noted. Sequence analysis of the IVD gene in the patient revealed the novel compound mutations-a missense mutation, c.986T>C (p.Met329Thr) and a frameshift mutation, c.1083del (p.Ile361fs*11). Following stabilization during the acute phase, the patient has remained in a stable condition on a low-leucine diet

Kaempferol inhibits IL‑1β‑induced proliferation of rheumatoid arthritis synovial fibroblasts and the production of COX‑2, PGE2 and MMPs

Inflammatory cytokines, matrix metalloproteinases (MMPs) and cyclooxygenase (COX)‑2 released from rheumatoid arthritis synovial fibroblasts (RASFs) are involved in the destruction of both articular bone and cartilage. Kaempferol has been reported to act as an antioxidant and anti‑inflammatory agent by inhibiting nitric oxide synthase and COX enzymes. The aim of the present study was to determine the effects of kaempferol on the interleukin‑1β (IL‑1β)‑induced proliferation of RASFs and the production of MMPs, COX and prostaglandin E2 (PGE2) by RASFs. The proliferation of the RASFs stimulated with IL‑1β and treated with/without kaempferol was evaluated by CCK‑8 assay. The expression of MMPs, TIMP metallopeptidase inhibitor‑1 (TIMP‑1), COXs, PGE2 and that of intracellular MAPK signaling molecules, including p‑ERK, p‑p38, p‑JNK and nuclear factor‑κB (NF‑κB) was examined by immunoblotting or semi‑quantitative reverse transcription‑polymerase chain reaction (RT‑PCR) and ELISA under the conditions described above. Kaempferol inhibited the proliferation of both unstimulated and IL‑1β‑stimulated RASFs, as well as the mRNA and protein expression of MMP‑1, MMP-3, COX‑2 and PGE2 induced by IL‑1β. Kaempferol also inhibited the phosphorylation of ERK‑1/2, p38 and JNK, as well as the activation of NF‑κB induced by IL‑1β. These results indicate that kaempferol inhibits synovial fibroblast proliferation, as well as the production of and MMPs, COX‑2 and PGE2, which is involved in articular inflammation and destruction in rheumatoid arthritis (RA). Our data suggest that kaempferol may be a novel therapeutic agent for the treatment of RA