Incidence of iatrogenic pneumothorax following acupuncture treatments in Taiwan.

BACKGROUND: Pneumothorax is a rare complication of acupuncture and the risk factors are unclear. OBJECTIVE: This study analysed the incidence of post-acupuncture pneumothorax requiring hospitalisation in a one-million-sample cohort derived from Taiwan's National Health Insurance Research Database. METHODS: We tracked this cohort between 1997 and 2012 and recorded all medical insurance information. Subjects were categorised according to gender, insurance amount, comorbidities, residential area, and number of acupuncture treatments. Pneumothorax risk was evaluated according to different demographic and medical variables by logistic regression analysis using an adjusted odds ratio (aOR) with a 95% confidence interval (95% CI). RESULTS: Overall, 411 734 patients undergoing 5 407 378 acupuncture treatments were identified with data collected over the first 7 days after acupuncture. The incidence rates of iatrogenic pneumothorax were 0.87 per 1 000 000 acupuncture treatments overall and 1.75 per 1 000 000 acupuncture treatments in "at-risk" anatomical areas. Multivariate logistic regression demonstrated that a history of thoracic surgery (aOR 7.85, 95% CI 3.49 to 9.25), chronic bronchitis (aOR 2.61, 95% CI 1.03 to 6.87), emphysema (aOR 4.87, 95% CI 1.03 to 7.96), pneumonia (aOR 2.09, 95% CI 1.44 to 2.72), tuberculosis (aOR 3.65, 95% CI 1.39 to 9.56), and lung cancer (aOR 3.85, 95% CI 1.53 to 9.73) may increase the post-acupuncture risk of iatrogenic pneumothorax. Men had a higher risk of pneumothorax than women (aOR 3.41, 95% CI 1.36 to 8.57). The number of treatments was not associated with risk of pneumothorax. CONCLUSIONS: Patients with a history of lung disease including chronic bronchitis, emphysema, tuberculosis, lung cancer and pneumonia, and a history of thoracic surgery, might have an increased post-acupuncture risk of pneumothorax. This information may possibly help physicians avoid post-acupuncture pneumothorax.

Propionate-induced changes in cardiac metabolism, notably CoA trapping, are not altered by l-carnitine.

High concentrations of propionate and its metabolites are found in several diseases that are often associated with the development of cardiac dysfunction, such as obesity, diabetes, propionic acidemia, and methylmalonic acidemia. In the present work, we employed a stable isotope-based metabolic flux approach to understand propionate-mediated perturbation of cardiac energy metabolism. Propionate led to accumulation of propionyl-CoA (increased by ~101-fold) and methylmalonyl-CoA (increased by 36-fold). This accumulation caused significant mitochondrial CoA trapping and inhibited fatty acid oxidation. The reduced energy contribution from fatty acid oxidation was associated with increased glucose oxidation. The enhanced anaplerosis of propionate and CoA trapping altered the pool sizes of tricarboxylic acid cycle (TCA) metabolites. In addition to being an anaplerotic substrate, the accumulation of proprionate-derived malate increased the recycling of malate to pyruvate and acetyl-CoA, which can enter the TCA for energy production. Supplementation of 3 mM l-carnitine did not relieve CoA trapping and did not reverse the propionate-mediated fuel switch. This is due to new findings that the heart appears to lack the specific enzyme catalyzing the conversion of short-chain (C3 and C4) dicarboxylyl-CoAs to dicarboxylylcarnitines. The discovery of this work warrants further investigation on the relevance of dicarboxylylcarnitines, especially C3 and C4 dicarboxylylcarnitines, in cardiac conditions such as heart failure.

[Effects of Nutrient Inputs on Changes of Phosphorus Forms and Phytoplankton Growth in Taihu Lake].

In order to determine the effects of nutrient inputs on changes of phosphorus forms and phytoplankton growth in large shallow lakes, an enrichment bioassay was conducted using surface lake water collected from the Meiliang Bay of Taihu Lake in spring. The concentration of different phosphorus forms, phytoplankton biomass (chlorophyll a) and alkaline phosphatase activity (APA) was analyzed after the addition of different concentrations of inorganic nutrients. The results showed that the phytoplankton biomass increased significantly with the addition of phosphorus (P), but with no primary effect from nitrogen (N), which suggested the phytoplankton growth was mainly limited by P. The maximum growth rate and the highest concentration of chlorophyll both occurred in the SRP 0.015 mg x L(-1) treatment. Nitrate addition could improve the bioavailability of phosphorus, accelerate the phosphorus cycling process and promote the growth of APA. There was an induction-repression mechanism resulting in a negative relationship between APA and orthophosphate concentration. The APA was obviously stimulated under PO4(3-) -P ≤ 0.025 mg x L(-1). This paper researches the transformation and cycling process of phosphorus in water and the induction-repression mechanism between the APA and orthophosphate concentration. The result can help to reveal the compensation path of nutrients in algae growth process and provide a theoretical basis for the further reveal of the mechanism of algae outbreaks.

Polarization of natural killer T cells towards an NKT2 subpopulation occurs after stimulation with alpha-galactosylceramide and rhG-CSF in aplastic anemia.

Natural killer T (NKT) cells play an important role in the regulation of immune responses in a broad range of diseases, including autoimmune disorders, infectious diseases and cancer. So far, few studies have evaluated the roles of NKT cells in the pathogenesis of aplastic anemia (AA), an autoimmune disease. In this study, we investigated the quantitative and qualitative changes in NKT cells in bone marrow (BM) mononuclear cells of AA patients in response to in vitro stimulation with alpha-galactosylceramide. Compared to healthy controls, BM from AA patients had reduced fraction of NKT cells, which possessed a decreased potential to expand in vitro in response to alpha-galactosylceramide stimulation, producing more IFNgamma+ NKT1 cells. In the presence of rhG-CSF, the expansion capacity of NKT cells stimulated by alpha-galactosylceramide was significantly reduced in both AA and control groups, with the majority of the activated NKT cells expressing intracellular IL-4, and the fractions of IFNgamma+ NKT cells were significantly reduced. In summary, our results indicate that polarization of NKT cells towards the NKT2 subpopulation occurs after co-stimulation with alpha-galactosylceramide and rhG-CSF in AA.