Admission Norton scale scores (ANSS) correlate with rehabilitation outcome and length in elderly patients with deconditioning

We sought to determine if admission Norton scale scores (ANSS) used for evaluating pressure ulcer risk also correlate with rehabilitation outcome and length in elderly patients with deconditioning. This was a retrospective study conducted in a geriatric department between June 2008 and June 2010. The medical charts of consecutive elderly (≥65 years) patients admitted for rehabilitation due to deconditioning were studied for the following measurements: ANSS, admission albumin serum levels, mini-mental status examination (MMSE) scores, discharge walking functional independence measure (FIM) scores, discharge transfer FIM scores, and rehabilitation length. The cohort included 152 patients: 79 (52%) females and 73 (48%) males. Mean age was 83.6±6.5 years. The three most common causes of deconditioning were pneumonia, congestive heart failure exacerbation, and falls. ANSS correlated with discharge walking FIM scores (r=0.32; p=0.003), discharge transfer FIM scores (r=0.30; p=0.005), and length of rehabilitation (r=-0.37; p<0.0001), following adjustment for age, albumin serum levels, and MMSE scores. Linear regression analysis showed that ANSS were independently associated with discharge walking FIM scores (p=0.004), discharge transfer FIM scores (p=0.006), and rehabilitation length (p<0.0001). We conclude that the Norton scoring system may be used for predicting the outcome and the length of rehabilitation in elderly patients with deconditioning.     

儿童牙科患者就诊行为状况和影响因素的分析

目的:调查分析儿童牙科患者就诊行为状况和不合作行为的相关因素。方法:采用问卷调查和改良的合作行为级别评定量表对257名儿童牙科就诊行为状况和相关因素进行调查,采用χ2检验进行单因素分析,并将具有统计学意义的因素进行二元logistic回归分析。结果:257例患儿不合作行为的发生率为23.3%。Logistic回归结果提示:儿童牙科患者不合作行为与就诊原因和患儿年龄密切相关。随着年龄增长,不合作行为发生减少。而就诊原因中的尖周炎是不合作行为的危险因素。结论:儿童牙科患者普遍存在不合作行为,就诊原因中的尖周炎和患儿的年龄是不合作行为的重要预测因子。     

全口义齿腭皱对语音恢复的作用

目的:研究金属基托全口义齿腭皱对修复后辅音声学特征的影响。方法:30例无牙颌患者分别戴入光滑面金属基托全口义齿(第一组)和有腭皱金属基托全口义齿(第二组),应用Minispeech lab测量并分析患者在初戴前,初戴时,初戴后1周、2周、4周、8周时汉语拼音/j/、/q/的第二强频区(F2)值、带宽(B2)值和嗓音起始时间(V.O.T.)。结果:第一组中,与初戴前相比,/j/、/q/的F2值从初戴后2周开始差异有统计学意义(P<0.05),/j/的B2值在初戴后8周,/q/的B2值在初戴后4周差异有统计学意义(P<0.05);第二组中,与初戴前相比,/j/、/q/的F2值从初戴后1周开始差异有统计学意义(P<0.05),/j/的B2值从初戴后2周开始,/q/的B2值从初戴后4周开始差异有统计学意义(P<0.05)。结论:金属基托全口义齿的腭皱能够缩短金属基托全口义齿初戴后患者语音恢复的时间。     

Mouse NK cell-mediated rejection of bone marrow allografts exhibits patterns consistent with Ly49 subset licensing

Natural killer (NK) cells can mediate the rejection of bone marrow allografts and exist as subsets based on expression of inhibitory/activating receptors that can bind MHC. In vitro data have shown that NK subsets bearing Ly49 receptors for self-MHC class I have intrinsically higher effector function, supporting the hypothesis that NK cells undergo a host MHC-dependent functional education. These subsets also play a role in bone marrow cell (BMC) allograft rejection. Thus far, little in vivo evidence for this preferential licensing across mouse strains with different MHC haplotypes has been shown. We assessed the intrinsic response potential of the different Ly49(+) subsets in BMC rejection by using β2-microglobulin deficient (β2m(-/-)) mice as donors. Using congenic and allogeneic mice as recipients and depleting the different Ly49 subsets, we found that NK subsets bearing Ly49s, which bind "self-MHC" were found to be the dominant subset responsible for β2m(-/-) BMC rejection. This provides in vivo evidence for host MHC class I-dependent functional education. Interestingly, all H2(d) strain mice regardless of background were able to resist significantly greater amounts of β2m(-/-), but not wild-type BMC than H2(b) mice, providing evidence that the rheostat hypothesis regarding Ly49 affinities for MHC and NK-cell function impacts BMC rejection capability.     

AAV8 vector expressing IL24 efficiently suppresses tumor growth mediated by specific mechanisms in MLL/AF4-positive ALL model mice

Mixed-lineage leukemia (MLL)/AF4-positive acute lymphoblastic leukemia (ALL) is a common type of leukemia in infants, which is associated with a high relapse rate and poor prognosis. IL24 selectively induces apoptosis in cancer cells and exerts immunomodulatory and antiangiogenic effects. We examined the effects of adeno-associated virus type 8 (AAV8) vector-mediated muscle-directed systemic gene therapy in MLL/AF4-positive ALL using IL24. In a series of in vitro studies, we examined the effects of AAV8-IL24-transduced C2C12 cell-conditioned medium. We also examined the effects of AAV8-IL24 in MLL/AF4 transgenic mice. The results revealed the effects of AAV8-IL24 in MLL/AF4-positive ALL both in vitro and in vivo. With regard to the mechanism of therapy using AAV8-IL24 in MLL/AF4-positive ALL, we demonstrated the antiangiogenicity and effects on the ER stress pathway and unreported pathways through inhibition of S100A6 and HOXA9, which is specific to MLL/AF4-positive ALL. Inhibition of S100A6 by IL24 was dependent on TNF-α and induced acetylation of p53 followed by activation of the caspase 8-caspase 3 apoptotic pathway. Inhibition of HOXA9 by IL24, which was independent of TNF-α, induced MEIS1 activation followed by activation of the caspase 8-caspase 3 apoptotic pathway. Thus, gene therapy using AAV8-IL24 is a promising treatment for MLL/AF4-positive ALL.     

Functional STAT3 deficiency compromises the generation of human T follicular helper cells

T follicular helper (Tfh) cells are critical for providing the necessary signals to induce differentiation of B cells into memory and Ab-secreting cells. Accordingly, it is important to identify the molecular requirements for Tfh cell development and function. We previously found that IL-12 mediates the differentiation of human CD4(+) T cells to the Tfh lineage, because IL-12 induces naive human CD4(+) T cells to acquire expression of IL-21, BCL6, ICOS, and CXCR5, which typify Tfh cells. We have now examined CD4(+) T cells from patients deficient in IL-12Rβ1, TYK2, STAT1, and STAT3 to further explore the pathways involved in human Tfh cell differentiation. Although STAT1 was dispensable, mutations in IL12RB1, TYK2, or STAT3 compromised IL-12-induced expression of IL-21 by human CD4(+) T cells. Defective expression of IL-21 by STAT3-deficient CD4(+) T cells resulted in diminished B-cell helper activity in vitro. Importantly, mutations in STAT3, but not IL12RB1 or TYK2, also reduced Tfh cell generation in vivo, evidenced by decreased circulating CD4(+)CXCR5(+) T cells. These results highlight the nonredundant role of STAT3 in human Tfh cell differentiation and suggest that defective Tfh cell development and/or function contributes to the humoral defects observed in STAT3-deficient patients.