Illegal births and legal abortions – the case of China

BACKGROUND: China has a national policy regulating the number of children that a woman is allowed to have. The central concept at the individual level application is "illegal pregnancy". The purpose of this article is to describe and problematicize the concept of illegal pregnancy and its use in practice. METHODS: Original texts and previous published and unpublished reports and statistics were used. RESULTS: By 1979 the Chinese population policy was clearly a policy of controlling population growth. For a pregnancy to be legal, it has to be defined as such according to the family-level eligibility rules, and in some places it has to be within the local quota. Enforcement of the policy has been pursued via the State Family Planning (FP) Commission and the Communist Party (CP), both of which have a functioning vertical structure down to the lowest administrative units. There are various incentives and disincentives for families to follow the policy. An extensive system has been created to keep the contraceptive use and pregnancy status of all married women at reproductive age under constant surveillance. In the early 1990s FP and CP officials were made personally responsible for meeting population targets. Since 1979, abortion has been available on request, and the ratio of legal abortions to birth increased in the 1980s and declined in the 1990s. Similar to what happens in other Asian countries with low fertility rates and higher esteem for boys, both national- and local-level data show that an unnaturally greater number of boys than girls are registered as having been born. CONCLUSION: Defining a pregnancy as "illegal" and carrying out the surveillance of individual women are phenomena unique in China, but this does not apply to other features of the policy. The moral judgment concerning the policy depends on the basic question of whether reproduction should be considered as an individual or social decision

Eficácia do exercício físico na fadiga dos pacientes com câncer durante o tratamento ativo: revisão sistemática e meta-análise

El objetivo del estudio fue determinar la efectividad del ejercicio físico en la fatiga de pacientes con cáncer durante el tratamiento activo. Las bases de datos de PubMed Central, EMBASE y OVID fueron consultadas hasta abril de 2014 para identificar ensayos clínicos aleatorizados, que evaluaran el efecto del ejercicio en la fatiga de pacientes con cáncer sometidos a tratamiento activo. Once estudios (n = 1.407) fueron incluidos. La quimioterapia fue el tratamiento más común (n = 1.028). Los estudios tuvieron bajo riesgo de sesgo y alta calidad metodológica. Las estimaciones de efecto mostraron que el ejercicio físico mejoró significativamente la fatiga (SMD = -3,0; IC95%: -5,21; -0,80), p < 0,0001. Se encontraron efectos similares para el entrenamiento de resistencia (SMD = -4,5; IC95%: -7,24; -1,82), p = 0,001. Se encontraron mejoras significativas en pacientes con cáncer de mama y de próstata (p < 0,05). El ejercicio es una intervención segura y eficaz en el control de la fatiga en pacientes sometidos a tratamiento activoThis study aimed to determine the effectiveness of physical exercise in decreasing fatigue in cancer patients during active treatment. The PubMed Central, EMBASE, and OVID databases were consulted up to April 2014 to identify randomized clinical trials that evaluated the effect of exercise on fatigue in cancer patients undergoing active treatment. Eleven studies (n = 1,407) were included. Chemotherapy was the most common form of treatment (n = 1,028). The studies showed a low risk of bias and high methodological quality. Effect estimates showed that physical exercise significantly improved fatigue (SMD = -3.0; 95%CI: -5.21; -0.80), p < 0.0001. Similar effects were found for resistance training (SMD = -4.5; 95%CI: -7.24; -1.82), p = 0.001. Significant improvements were found in breast and prostate cancer patients (p < 0.05). Exercise is a safe and effective intervention in the management fatigue in cancer patients undergoing active treatmentO objetivo foi determinar a efetividade do exercício físico sobre a fadiga em pacientes com câncer durante o tratamento ativo. As bases de dados PubMed Central, EMBASE e OVID foram consultadas até abril de 2014 para identificar ensaios clínicos randomizados que avaliaram o efeito do exercício sobre a fadiga em pacientes com câncer em tratamento ativo. Onze estudos (n = 1.407) foram incluídos. A quimioterapia foi o tratamento mais comum (n = 1.028). Os estudos tiveram baixo risco de viés e alta qualidade metodológica. As estimativas de efeito mostraram que o exercício melhorou significativamente a fadiga (DMP = -3,0; IC95%: -5,21; -0,80), p < 0,0001. Efeitos semelhantes sobre o treinamento de resistência (DMP = -4,5; IC95%: -7,24; -1,82), p = 0,001 foram encontrados. O exercício físico é uma intervenção segura e eficaz contra a fadiga em pacientes submetidos ao tratamento ativoEl presente trabajo forma parte del Proyecto Práctica del autoexamen de seno y los conocimientos, factores de riesgo y estilos de vida relacionados con el cáncer de mama en mujeres jóvenes de la Universidad Santo Tomás de Bogotá: un análisis transversal (9ª Convocatoria FODEIN- Código del proyecto 4110060001 - 008)

Mitochondrial hydrogen sulfide supplementation improves health in the C. elegans Duchenne muscular dystrophy model

This is the final version. Available on open access from the National Academy of Sciences via the DOI in this record. Data Availability: All study data are included in the article.Duchenne muscular dystrophy (DMD) is an X-linked recessive disorder characterized by progressive muscle degeneration and weakness due to mutations in the dystrophin gene. The symptoms of DMD share similarities with those of accelerated aging. Recently, hydrogen sulfide (H2S) supplementation has been suggested to modulate the effects of age-related decline in muscle function, and metabolic H2S deficiencies have been implicated in affecting muscle mass in conditions such as phenylketonuria. We therefore evaluated the use of sodium GYY4137 (NaGYY), a H2S-releasing molecule, as a possible approach for DMD treatment. Using the dys-1(eg33) Caenorhabditis elegans DMD model, we found that NaGYY treatment (100 µM) improved movement, strength, gait, and muscle mitochondrial structure, similar to the gold-standard therapeutic treatment, prednisone (370 µM). The health improvements of either treatment required the action of the kinase JNK-1, the transcription factor SKN-1, and the NAD-dependent deacetylase SIR-2.1. The transcription factor DAF-16 was required for the health benefits of NaGYY treatment, but not prednisone treatment. AP39 (100 pM), a mitochondria-targeted H2S compound, also improved movement and strength in the dys-1(eg33) model, further implying that these improvements are mitochondria-based. Additionally, we found a decline in total sulfide and H2S-producing enzymes in dystrophin/utrophin knockout mice. Overall, our results suggest that H2S deficit may contribute to DMD pathology, and rectifying/overcoming the deficit with H2S delivery compounds has potential as a therapeutic approach to DMD treatment.Medical Research Council (MRC)NASABiotechnology and Biological Sciences Research Council (BBSRC)Medical Research Council (MRC)United Mitochondrial Disease FoundationMRC Versus Arthritis Centre for Musculoskeletal Ageing ResearchNational Health and Medical Research CouncilUniversity of Nottingham School of MedicineFulbright U.S. Student ProgramGermanistic Society of AmericaBrian Ridge ScholarshipUniversity of ExeterUniversity of New South WalesUniversity of MelbourneRebecca L. Cooper Medical Research FoundationOsteopathic Heritage Foundatio

Study of the reaction e^{+}e^{-} -->J/psi\pi^{+}\pi^{-} via initial-state radiation at BaBar

We study the process $e^+e^-\to J/\psi\pi^{+}\pi^{-}$ with initial-state-radiation events produced at the PEP-II asymmetric-energy collider. The data were recorded with the BaBar detector at center-of-mass energies 10.58 and 10.54 GeV, and correspond to an integrated luminosity of 454 $\mathrm{fb^{-1}}$. We investigate the $J/\psi \pi^{+}\pi^{-}$ mass distribution in the region from 3.5 to 5.5 $\mathrm{GeV/c^{2}}$. Below 3.7 $\mathrm{GeV/c^{2}}$ the $\psi(2S)$ signal dominates, and above 4 $\mathrm{GeV/c^{2}}$ there is a significant peak due to the Y(4260). A fit to the data in the range 3.74 -- 5.50 $\mathrm{GeV/c^{2}}$ yields a mass value $4244 \pm 5$ (stat) $\pm 4$ (syst)$\mathrm{MeV/c^{2}}$ and a width value $114 ^{+16}_{-15}$ (stat)$\pm 7$(syst)$\mathrm{MeV}$ for this state. We do not confirm the report from the Belle collaboration of a broad structure at 4.01 $\mathrm{GeV/c^{2}}$. In addition, we investigate the $\pi^{+}\pi^{-}$ system which results from Y(4260) decay

Recombinant human erythropoietin α modulates the effects of radiotherapy on colorectal cancer microvessels

Recent data suggest that recombinant human erythropoietin (rhEPO) modulates tumour growth and therapy response. The purpose of the present study was to examine the modulation of radiotherapy (RT) effects on tumour microvessels by rhEPO in a rat colorectal cancer model. Before and after 5 × 5 Gy of RT, dynamic contrast-enhanced -magnetic resonance imaging was performed and endothelial permeability surface product (PS), plasma flow (F), and blood volume (V) were modelled. Imaging was combined with pO2 measurements, analysis of microvessel density, microvessel diameter, microvessel fractal dimension, and expression of vascular endothelial growth factor (VEGF), hypoxia-inducible factor-1 α (HIF-1α), Bax, and Bcl-2. We found that RT significantly reduced PS and V in control rats, but not in rhEPO-treated rats, whereas F was unaffected by RT. Oxygenation was significantly better in rhEPO-treated animals, and RT induced a heterogeneous reoxygenation in both groups. Microvessel diameter was significantly larger in rhEPO animals, whereas VEGF expression was significantly lower in the rhEPO group. No differences were observed in HIF-1α, Bax, or Bcl-2 expression. We conclude that rhEPO results in spatially heterogeneous modulation of RT effects on tumour microvessels. Direct effects of rhEPO on neoplastic endothelium are likely to explain these findings in addition to indirect effects induced by increased oxygenation

The effects of traditional, superset, and tri-set resistance training structures on perceived intensity and physiological responses.

PURPOSE: Investigate the acute and short-term (i.e., 24 h) effects of traditional (TRAD), superset (SS), and tri-set (TRI) resistance training protocols on perceptions of intensity and physiological responses. METHODS: Fourteen male participants completed a familiarisation session and three resistance training protocols (i.e., TRAD, SS, and TRI) in a randomised-crossover design. Rating of perceived exertion, lactate concentration ([Lac]), creatine kinase concentration ([CK]), countermovement jump (CMJ), testosterone, and cortisol concentrations was measured pre, immediately, and 24-h post the resistance training sessions with magnitude-based inferences assessing changes/differences within/between protocols. RESULTS: TRI reported possible to almost certainly greater efficiency and rate of perceived exertion, although session perceived load was very likely lower. SS and TRI had very likely to almost certainly greater lactate responses during the protocols, with changes in [CK] being very likely and likely increased at 24 h, respectively. At 24-h post-training, CMJ variables in the TRAD protocol had returned to baseline; however, SS and TRI were still possibly to likely reduced. Possible increases in testosterone immediately post SS and TRI protocols were reported, with SS showing possible increases at 24-h post-training. TRAD and SS showed almost certain and likely decreases in cortisol immediately post, respectively, with TRAD reporting likely decreases at 24-h post-training. CONCLUSIONS: SS and TRI can enhance training efficiency and reduce training time. However, acute and short-term physiological responses differ between protocols. Athletes can utilise SS and TRI resistance training, but may require additional recovery post-training to minimise effects of fatigue

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.