Near-linear response of mean monsoon strength to a broad range of radiative forcings

Theoretical models have been used to argue that seasonal mean monsoons will shift abruptly and discontinuously from wet to dry stable states as their radiative forcings pass a critical threshold, sometimes referred to as a “tipping point.” Further support for a strongly nonlinear response of monsoons to radiative forcings is found in the seasonal onset of the South Asian summer monsoon, which is abrupt compared with the annual cycle of insolation. Here it is shown that the seasonal mean strength of monsoons instead exhibits a nearly linear dependence on a wide range of radiative forcings. First, a previous theory that predicted a discontinuous, threshold response is shown to omit a dominant stabilizing term in the equations of motion; a corrected theory predicts a continuous and nearly linear response of seasonal mean monsoon strength to forcings. A comprehensive global climate model is then used to show that the seasonal mean South Asian monsoon exhibits a near-linear dependence on a wide range of isolated greenhouse gas, aerosol, and surface albedo forcings. This model reproduces the observed abrupt seasonal onset of the South Asian monsoon but produces a near-linear response of the mean monsoon by changing the duration of the summer circulation and the latitude of that circulation’s ascent branch. Thus, neither a physically correct theoretical model nor a comprehensive climate model support the idea that seasonal mean monsoons will undergo abrupt, nonlinear shifts in response to changes in greenhouse gas concentrations, aerosol emissions, or land surface albedo.Monsoons deliver water to billions of people, so catastrophe would likely result if a gradual and small change in a forcing produced a comparatively abrupt and large change in monsoon strength. Previous studies (1, 2) used theoretical models to argue that monsoons will undergo exactly this sort of abrupt transition if anthropogenic or natural forcings exceed a critical threshold, which they referred to as a “tipping point” (3). Changes in land use or atmospheric aerosols sufficient to increase local top-of-atmosphere albedo to 0.5 have been predicted to cause a shift in the Indian summer monsoon from its current wet state to a dry state (1). The idea that anthropogenic climate forcings might produce an abrupt shutdown of some monsoons has become prominent (3, 4), even though some argue that this is unlikely to occur in the next century (5).Paleoclimate records contain abundant evidence for abrupt changes in various measures of monsoon strength (6, 7). However, such records typically measure variations at a particular location and so may not distinguish between a nonlinear response of the entire monsoon and a more gradual, linear shift of a spatial pattern with sharp horizontal gradients. It is also unclear whether mechanisms that govern monsoon changes on orbital to geological time scales are relevant for the response to anthropogenic forcings. However, even if proxy records of past monsoons are ambiguous, the modern seasonal cycle contains evidence for the abrupt response of monsoons to a radiative forcing: South Asian summer monsoon onset occurs more rapidly than can be explained by a linear response to the annual cycle of insolation (8, 9). Although the cause of this nonlinear seasonal evolution is the subject of active research (10, 11), it seems plausible that the same mechanism might produce an abrupt response of the seasonal mean monsoon to an imposed seasonal mean forcing.These results motivate our examination of how monsoon strength scales with a range of forcings. In particular, we use a simple energetic theory and an ensemble of global climate model (GCM) integrations to determine whether the summer mean strength of tropical monsoons will change discontinuously in response to a large range of radiative forcings.     

Interleukin-6 enhances growth factor-dependent proliferation of the blast cells of acute myeloblastic leukemia

The effects of recombinant interleukin-6 (IL-6) on the proliferation of blast precursors present in the peripheral blood of patients with acute myeloblastic leukemia (AML) was investigated. IL-6 had little effect by itself; however, it synergized with granulocyte macrophage colony- stimulating factor (GM-CSF) and interleukin-3 (IL-3) in the stimulation of AML blast colony formation. Responsiveness of blast progenitors to IL-6 was heterogeneous. On normal bone marrow cells the same synergy was observed on granulocyte and monocyte precursors (GM-CFC), while there was no significant effect on erythroid and multipotential precursors.     

6q deletions define distinct clinico-pathologic subsets of non- Hodgkin's lymphoma

Commonly observed in lymphoid neoplasms, deletions of 6q have been correlated with histologic and clinical subsets of non-Hodgkin's lymphoma (NHL). Our recent analysis of loss of heterozygosity of 6q loci in NHL showed two regions of minimal molecular deletion (RMD), an RMD1 at 6q25-27 and an RMD2 at 6q21-23. To establish correlations between these RMDs and regions of minimal cytogenetic deletions (RCDs) on 6q, and to define associations between RCDs and clinico-pathologic features, we have analyzed chromosome 6 abnormalities in 459 consecutively ascertained, karyotypically abnormal cases of NHL. Among these, 126 (27.5%) cases had structural abnormalities of chromosome 6, of which 94 were deletions. Analysis of these deletions identified three RCDs. An RCD1 encompassing 6q25-27 was seen in 45 intermediate- grade NHL. An RCD2 at 6q21 was observed in 11 high-grade NHL, 9 of which were of the immunoblastic subtype. An RCD3 at 6q23 was noted in 18 low-grade NHL lacking a t(14;18) translocation. Of these 18 cases, 12 were small lymphocytic NHL and, in 2 of these, del(6q) was the sole karyotypic abnormality. In 20 cases of low-grade NHL with t(14;18), the deletions spanned both RCD1 and RCD3. These data suggested the presence of at least 3 tumor suppressor genes on 6q within RCD1, RCD2, and RCD3; they also showed associations between RCDs in 6q and subsets of NHL, including a specific association between a group of well-differentiated lymphoid neoplasms and RCD3. The apparent heterogeneity of breakpoints when all NHLs are considered together explains the inability of previous studies to reliably establish correlations between recurring 6q deletions and histologic and clinical features of NHL.     

The toxicity of very prolonged courses of PEGasparaginase or Erwinia asparaginase in relation to asparaginase activity,with a special focus on dyslipidemia

We prospectively studied the incidence and clinical course of hypertriglyceridemia and hypercholesterolemia during very prolonged use of asparaginase in relation to levels of asparaginase activity in children with acute lymphoblastic leukemia. We also evaluated the incidence of pancreatitis, thrombosis, hyperammonemia and central neurotoxicity and their association with asparaginase activity levels. Eighty-nine patients were treated according to the Dutch Childhood Oncology Group Acute Lymphoblastic Leukemia 10 medium-risk intensification protocol, which includes 15 doses of PEGasparaginase (2,500 IU/m²) over 30 weeks. Erwinia asparaginase (20,000 IU/m²) was administered when allergy to or silent inactivation of PEGasparaginase occurred. Triglyceride, cholesterol and ammonia levels increased rapidly in children treated with PEGasparaginase and remained temporarily elevated, but normalized after administration of the last asparaginase dose. Among the patients treated with PEGasparaginase, hypertriglyceridemia and hypercholesterolemia (grade 3/4) were found in 47% and 25%, respectively. The correlation between PEGasparaginase activity levels and triglyceride levels was strongest at week 5 (Spearman correlation coefficient=0.36, P=0.005). The triglyceride levels were higher in children ≥10 years old than in younger patients (<10 years old) after adjustment for type of asparaginase preparation: median 4.9 mmol/L versus 1.6 mmol/L (P<0.001). In patients receiving Erwinia asparaginase, triglyceride levels increased in the first weeks as well, but no grade 3/4 dyslipidemia was found. Hyperammonemia (grade 3/4) was only found in patients treated with Erwinia asparaginase (9%). Thrombosis occurred in 4.5%, pancreatitis in 7%, and central neurotoxicity in 9% of patients using either of the two agents; these toxicities were not related to levels of asparaginase activity or to triglyceride levels. In conclusion, severe dyslipidemia occurred frequently, but was temporary and was not associated with relevant clinical events and should not, therefore, be considered a reason for modifying asparaginase treatment. Dyslipidemia was the only toxicity related to levels of asparaginase activity.     

Evaluation of the impact of organ-specific dose reduction on image quality in pediatric chest computed tomography

Background

Organ-specific dose reduction significantly reduces the radiation exposure of radiosensitive organs.

Objective

The purpose of this study was to assess the impact of a novel organ-specific dose reduction algorithm on image quality of pediatric chest CT.

Materials and methods

We included 28 children (mean age 10.9?±?4.8 years, range 3–18 years) who had contrast-enhanced chest CT on a 128-row scanner. CT was performed at 100 kV using automated tube current modulation and a novel organ-specific dose-reduction algorithm (XCare?; Siemens, Forchheim, Germany). Seven children had a previous chest CT performed on a 64-row scanner at 100 kV without organ-specific dose reduction. Subjective image quality was assessed using a five-point scale (1-not diagnostic; 5-excellent). Contrast-to-noise ratio (CNR) and signal-to-noise ratio (SNR) were assessed in the descending aorta.

Results

Overall mean subjective image quality was 4.1?±?0.6. In the subgroup of the seven children examined both with and without organ-specific dose reduction, subjective image quality was comparable (score 4.4?±?0.5 with organ-specific dose reduction vs. 4.4?±?0.7 without it; P?>?0.05). There was no significant difference in mean signal-to-noise ratio and contrast-to-noise ratio with organ-specific dose reduction (38.3?±?10.1 and 28.5?±?8.7, respectively) and without the reduction (35.5?±?8.5 and 26.5?±?7.8, respectively) (P?>?0.05). Volume computed tomography dose index (CTDI_vol) and size-specific dose estimates did not differ significantly between acquisitions with the organ-specific dose reduction (1.7?±?0.8 mGy) and without the reduction (1.7?±?0.8 mGy) (P?>?0.05).

Conclusion

Organ-specific dose reduction does not have an impact on image quality of pediatric chest CT and can therefore be used in clinical practice to reduce radiation dose of radiosensitive organs such as breast and thyroid gland.     

胃、结直肠癌术前区域性动脉化疗几个相关问题

胃、结直肠癌根治性切除术复发转移是严重影响术后5 a生存率提高的重要原因.以手术为主综合治疗已成为新的趋势,其中术前区域性动脉化疗(preoperative regional-arterial chemotherapy,PRAC)尤为值得重视.本文介绍了术前PRAC的概念、作用机制和影响区域性动脉化疗疗效的相关因素,并就术前区域性动脉化疗在胃、结直肠癌综合治疗中的评价进行讨论.     

清开灵与利巴韦林治疗小儿呼吸道合胞病毒肺炎的比较：单盲、随机、平行对照试验

目的:比较清开灵与利巴韦林对呼吸道合胞病毒肺炎患儿治疗效果的差异。方法:选择2005-02/2006-04在北京儿童医院分中心治疗的小儿呼吸道合胞病毒肺炎97例,患儿法定监护人知情同意。采用单盲、随机、平行对照试验的原则,按区组随机化方法分为2组,清开灵注射液组49例,利巴韦林组48例。①清开灵注射液组:清开灵注射液静脉滴注加口服中成药。②利巴韦林组:利巴韦林注射液静脉滴注加口服复方愈创木酚磺酸钾口服液。两组疗程均为10d,比较两组患儿的疗效。结果:清开灵注射液组脱落3例,利巴韦林组脱落1例,进入结果分析清开灵注射液组46例,利巴韦林组47例。①清开灵注射液组发热患儿体温恢复正常时间比利巴韦林组短[(2.72±1.86)d,(6.29±2.41)d(P<0.01)]。②清开灵注射液组患儿咳嗽、痰壅、气促症状积分改善方面优于利巴韦林组(P<0.05～0.01)。③清开灵注射液组的呼吸道合胞病毒转阴时间明显优于利巴韦林组。④咳嗽、痰壅、病毒转阴时间、气促均进入Logistic模型,其中前两个症状的回归系数绝对值较大。结论:清开灵注射液治疗小儿呼吸道合胞病毒肺炎在退热、止咳平喘、呼吸道合胞病毒转阴时间等方面均具有明显优势,咳嗽、痰壅这两个症状更能反映清开灵注射液的疗效优于利巴韦林。     

Biological treatment strategies for disc degeneration: potentials and shortcomings

Recent advances in molecular biology, cell biology and material sciences have opened a new emerging field of techniques for the treatment of musculoskeletal disorders. These new treatment modalities aim for biological repair of the affected tissues by introducing cell-based tissue replacements, genetic modifications of resident cells or a combination thereof. So far, these techniques have been successfully applied to various tissues such as bone and cartilage. However, application of these treatment modalities to cure intervertebral disc degeneration is in its very early stages and mostly limited to experimental studies in vitro or in animal studies. We will discuss the potential and possible shortcomings of current approaches to biologically cure disc degeneration by gene therapy or tissue engineering. Despite the increasing number of studies examining the therapeutic potential of biological treatment strategies, a practicable solution to routinely cure disc degeneration might not be available in the near future. However, knowledge gained from these attempts might be applied in a foreseeable future to cure the low back pain that often accompanies disc degeneration and therefore be beneficial for the patient. This study was supported by a grant from the AO Spine (SRN 02/103).