Chinese approaches to institutionalizing regional multilateralism

Over the last few years, China has promoted all kinds of regional and sub-regional cooperation in Asia. However, the extent of China’s drive for institutionalization of cooperative regional multilateral processes is limited by two realist considerations: I) Distribution of power among the forum participants, and whether the major players are well-disposed towards China or not so and II) the importance of the issues that the specific forum is set up to deal with, particularly to the political, economic or security interests of China, but also that of other participating states. China has successfully pushed for a high degree of institutionalization with the Shanghai Cooperation Organization (SCO) because the only other major participant (Russia) is a friend, and members have a salient accord in pursuing the aims of anti-terrorism and trade promotion. The Six-Party Talks (6PT) is minimally institutionalized because, although the issue of nuclear disarmament of North Korea is important to China, there are many heavy players with their own agenda in the forum (U.S., Japan, and Russia), North Korea itself is a maverick, and the participants have yet to take concrete steps in resolving many issues pertaining to North Korea giving up its nuclear weapons program. The semi-institutionalized character of the ASEAN+3 reflects the consultative nature of the forum that leaders of the Association of Southeast Asian Nations (ASEAN) and China, Japan and South Korea have decided upon, and competition for influence between China and Japan. To increase cooperation with ASEAN without the presence of foreign powers, China has worked towards institutionalizing a separate China-ASEAN axis within the rubric of ASEAN+3

A novel method to identify cooperative functional modules: study of module coordination in the Saccharomyces cerevisiae cell cycle

<p>Abstract</p> <p>Background</p> <p>Identifying key components in biological processes and their associations is critical for deciphering cellular functions. Recently, numerous gene expression and molecular interaction experiments have been reported in <it>Saccharomyces cerevisiae</it>, and these have enabled systematic studies. Although a number of approaches have been used to predict gene functions and interactions, tools that analyze the essential coordination of functional components in cellular processes still need to be developed.</p> <p>Results</p> <p>In this work, we present a new approach to study the cooperation of functional modules (sets of functionally related genes) in a specific cellular process. A cooperative module pair is defined as two modules that significantly cooperate with certain functional genes in a cellular process. This method identifies cooperative module pairs that significantly influence a cellular process and the correlated genes and interactions that are essential to that process. Using the yeast cell cycle as an example, we identified 101 cooperative module associations among 82 modules, and importantly, we established a cell cycle-specific cooperative module network. Most of the identified module pairs cover cooperative pathways and components essential to the cell cycle. We found that 14, 36, 18, 15, and 20 cooperative module pairs significantly cooperate with genes regulated in early G1, late G1, S, G2, and M phase, respectively. Fifty-nine module pairs that correlate with Cdc28 and other essential regulators were also identified. These results are consistent with previous studies and demonstrate that our methodology is effective for studying cooperative mechanisms in the cell cycle.</p> <p>Conclusions</p> <p>In this work, we propose a new approach to identifying condition-related cooperative interactions, and importantly, we establish a cell cycle-specific cooperation module network. These results provide a global view of the cell cycle and the method can be used to discover the dynamic coordination properties of functional components in other cellular processes.</p

Neuronal degeneration in autonomic nervous system of Dystonia musculorum mice

<p>Abstract</p> <p>Background</p> <p><it>Dystonia musculorum </it>(<it>dt</it>) is an autosomal recessive hereditary neuropathy with a characteristic uncoordinated movement and is caused by a defect in the <it>bullous pemphigoid antigen 1 </it>(<it>BPAG1</it>) gene. The neural isoform of <it>BPAG1 </it>is expressed in various neurons, including those in the central and peripheral nerve systems of mice. However, most previous studies on neuronal degeneration in <it>BPAG1</it>-deficient mice focused on peripheral sensory neurons and only limited investigation of the autonomic system has been conducted.</p> <p>Methods</p> <p>In this study, patterns of nerve innervation in cutaneous and iridial tissues were examined using general neuronal marker protein gene product 9.5 via immunohistochemistry. To perform quantitative analysis of the autonomic neuronal number, neurons within the lumbar sympathetic and parasympathetic ciliary ganglia were calculated. In addition, autonomic neurons were cultured from embryonic <it>dt/dt </it>mutants to elucidate degenerative patterns <it>in vitro</it>. Distribution patterns of neuronal intermediate filaments in cultured autonomic neurons were thoroughly studied under immunocytochemistry and conventional electron microscopy.</p> <p>Results</p> <p>Our immunohistochemistry results indicate that peripheral sensory nerves and autonomic innervation of sweat glands and irises dominated degeneration in <it>dt/dt </it>mice. Quantitative results confirmed that the number of neurons was significantly decreased in the lumbar sympathetic ganglia as well as in the parasympathetic ciliary ganglia of <it>dt/dt </it>mice compared with those of wild-type mice. We also observed that the neuronal intermediate filaments were aggregated abnormally in cultured autonomic neurons from <it>dt/dt </it>embryos.</p> <p>Conclusions</p> <p>These results suggest that a deficiency in the cytoskeletal linker BPAG1 is responsible for dominant sensory nerve degeneration and severe autonomic degeneration in <it>dt/dt </it>mice. Additionally, abnormally aggregated neuronal intermediate filaments may participate in neuronal death of cultured autonomic neurons from <it>dt/dt </it>mutants.</p

Clinical Impacts of Delayed Diagnosis of Hirschsprung’s Disease in Newborn Infants

BackgroundAsian infants are at a higher risk of having Hirschsprung’s disease (HD). Although HD is surgically correctable, serious and even lethal complications such as Hirschsprung’s-associated enterocolitis (HAEC) can still occur. The aim of this study was to investigate the risk factors of HAEC, and the clinical impacts of delayed diagnosis of HD in newborn infants.Patients and methodsBy review of medical charts in a medical center in Taiwan, 51 cases of neonates with HD between 2002 and 2009 were collected. Patients were divided into two groups based on the time of initial diagnosis: Group I, diagnosis made within 1 week after birth, and Group II after 1 week. Clinical features including demographic distribution, presenting features of HD, short-term and long-term complications related to HD were compared between the two groups of patients.ResultsThere were 25 patients in Group I and 19 in Group II. Group II patients had more severe clinical signs and symptoms of HAEC than Group I patients. The incidence of preoperative HAEC was 12% in Group I and 63% in Group II (adjusted odds ratio = 12.81, confidence interval = 2.60–62.97). Patients with preoperative HAEC were more likely to develop adhesive bowel obstruction after operation (33% vs. 3%, p = 0.013) and failure to thrive (33% vs. 3%, p = 0.013). Also, patients with long-segment or total colonic aganglionosis were at risk of developing both postoperative HAEC (85% vs. 29%, p = 0.001) and failure to thrive (39% vs. 3%, p = 0.002).ConclusionIn our study, we found that delayed diagnosis of HD beyond 1 week after birth significantly increases the risk of serious complications in neonatal patients. Patients with long-segment or total colonic aganglionosis have higher risk of postoperative HAEC and failure to thrive. Patients with preoperative HAEC are more likely to have adhesive bowel obstruction and failure to thrive

Renal Protection for Coronary Angiography in Advanced Renal Failure Patients by Prophylactic Hemodialysis A Randomized Controlled Trial

ObjectivesWe performed a study to determine whether prophylactic hemodialysis reduces contrast nephropathy (CN) after coronary angiography in advanced renal failure patients.BackgroundPre-existing renal failure is the greatest risk factor for CN. Hemodialysis can effectively remove contrast media, but its effect upon preventing CN is still uncertain.MethodsEighty-two patients with chronic renal failure, referred for coronary angiography, were assigned randomly to receive either normal saline intravenously and prophylactic hemodialysis (dialysis group; n = 42) or fluid supplement only (control group; n = 40).ResultsProphylactic hemodialysis lessened the decrease in creatinine clearance within 72 h in the dialysis group (0.4 ± 0.9 ml/min/1.73 m2vs. 2.2 ± 2.8 ml/min/1.73 m2; p < 0.001). Compared with the dialysis group, the serum creatinine concentrations in the control group were significantly higher at day 4 (6.3 ± 2.3 mg/dl vs. 5.1 ± 1.3 mg/dl; p = 0.010) and at peak level (6.7 ± 2.7 mg/dl vs. 5.3 ± 1.5 mg/dl; p = 0.005). Temporary renal replacement therapy was required in 35% of the control patients and in 2% of the dialysis group (p < 0.001). Thirteen percent of the control patients, but none of the dialysis patients, required long-term dialysis after discharge (p = 0.018). For the patients not requiring chronic dialysis, 13 patients in the control group (37%) and 2 in the dialysis group (5%) had an increase in serum creatinine concentration at discharge of more than 1 mg/dl from baseline (p < 0.001).ConclusionsProphylactic hemodialysis is effective in improving renal outcome in chronic renal failure patients undergoing coronary angiography