Impact of Adjuvant Radiotherapy on Survival after Pancreatic Cancer Resection: An Appraisal of Data from the National Cancer Data Base

Purpose

The impact of adjuvant radiotherapy for pancreatic adenocarcinoma (PAC) remains controversial. We examined effects of adjuvant therapy on overall survival (OS) in PAC, using the National Cancer Data Base (NCDB).

Methods

Patients with resected PAC from 1998 to 2002 were queried from the NCDB. Factors associated with receipt of adjuvant chemotherapy (ChemoOnly) versus adjuvant chemoradiotherapy (ChemoRad) versus no adjuvant treatment (NoAdjuvant) were assessed. Cox proportional hazard modeling was used to examine effect of adjuvant therapy type on OS. Propensity scores (PS) were developed for each treatment arm and used to produce matched samples for analysis to minimize selection bias.

Results

From 1998 to 2002, a total of 11,526 patients underwent resection of PAC. Of these, 1,029 (8.9 %) received ChemoOnly, 5,292 (45.9 %) received ChemoRad, and 5,205 (45.2 %) received NoAdjuvant. On univariate analysis, factors associated with improved OS included: younger age, higher income, higher facility volume, lower tumor stage and grade, negative margins and nodes, and absence of adjuvant therapy. On multivariate analysis with matched PS, factors independently associated with improved OS included: younger age, higher income, higher facility volume, later year of diagnosis, smaller tumor size, lower tumor stage, and negative tumor margins and nodes. ChemoRad had the best OS (hazard ratio 0.70, 95 % confidence interval 0.61–0.80) in a PS matched comparison with ChemoOnly (hazard ratio 1.04, 95 % confidence interval 0.93–1.18) and NoAdjuvant (index).

Conclusions

Adjuvant chemotherapy with radiotherapy is associated with improved OS after PAC resection in a large population from the NCDB. On the basis of these analyses, radiotherapy should be a part of adjuvant therapy for PAC.     

胶质瘤干细胞研究进展

随着对肿瘤干细胞（tumor stem cells）理论的深入认识和分离、培养肿瘤干细胞实验技术的不断进步,胶质瘤内肿瘤干细胞的存在已经有较多的证据和研究。这方面的研究不仅有助于深化人们对胶质瘤发生、复发和侵袭机制的认识,更重要的是可能改变以往胶质瘤的治疗策略,影响十分深远。新近,有学者将来自胶质瘤的肿瘤干细胞或具有干细胞特性的胶质瘤细胞称为“胶质瘤干细胞（glioma stem cells,GSC）”,较好地反映了这类细胞的特性。     

70岁以上住院老年慢性病病人抑郁和焦虑的调查

随着医学科学技术的飞速发展和人民物质精神生活水平的日益提高，我国人口的平均预期寿命不断增长，现已接近70岁。据统计：目前我国老年病人口（我国以60岁以上为老年病人）总数已近I．3亿，约占总人口数的10．09％，而75岁以上老年病人以每年平均3．62％的速度增长，预测到2025年将上升到20％，2050年将达到顶峰25．5％。老年人是慢性病的主要患病人群。因此，本研究针对70岁以上患慢性病的住院普通老年人和住院离休干部进行调查，采用Brink老年抑郁量表（GDS）、Zung焦虑自评量表（SAS），以了解住院老年人中存在的焦虑、抑郁情况以及分析两组病人的性别、年龄、文化程度、婚姻状况、个人习惯和经济收入情况。现将结果报道如下。[第一段]     

289 例特殊患者用药咨询调查分析

目的促进医院药房药师针对特殊人群的用药咨询工作质量。方法选择医院门诊289例特殊人员（孕妇、老人、未成年人监护人）用药咨询记录进行调查。结果与结论做好药房门诊的特殊患者用药咨询工作,可帮助患者提高合理、正确用药知识,从正确用药、减少误服和超量用药、不规范用药等方面起到辅助医疗作用。     

Clinical observation on hearing conditions of centenarians in northern district of China

Conclusion: The hearing conditions of the centenarians were quite poor as regards hearing thresholds and speech detection ability. Objective: To investigate hearing conditions of centenarians. Methods: A total of 54 centenarians in Rizhao and Linyi Districts in Shandong Province were investigated to assess hearing conditions of centenerians comprehensively by questionnaire investigation, pure-tone audiometry, acoustic immitance, intelligence evaluation, and speech detection scores. Also, 135 individuals were recruited as controls and divided into four groups according to their age: 45–59 years, 60–69 years, 70–79 years, and 80–89 years. Results: The hearing thresholds of the centenarians were dramatically higher than those of the control group (p < 0.05) and all centenarians suffered moderate to profound hearing loss according to the World Health Organization (WHO) criteria. Few centenarians had normal level of speech detection scores. All centenarians showed descending hearing curve, and the hearing threshold of the male centenarians at 8000 Hz was higher than that of the females (p = 0.047). There was a significant air–bone conduction gap in the centenarians (p < 0.05).     

18F-FDG PET/CT in lung adenosquamous carcinoma and its correlation with clinicopathological features and prognosis

Annals of Nuclear Medicine - Lung adenosquamous carcinoma (ASC) is a rare histological subtype of non-small cell lung cancer (NSCLC). Due to its rarity, the studies about 18F-FDG PET/CT in this...     

Selective degeneration of a physiological subtype of spinal motor neuron in mice with SOD1-linked ALS

Amyotrophic lateral sclerosis (ALS; Lou Gehrig’s disease) affects motor neurons (MNs) in the brain and spinal cord. Understanding the pathophysiology of this condition seems crucial for therapeutic design, yet few electrophysiological studies in actively degenerating animal models have been reported. Here, we report a novel preparation of acute slices from adult mouse spinal cord, allowing visualized whole cell patch-clamp recordings of fluorescent lumbar MN cell bodies from ChAT-eGFP or superoxide dismutase 1-yellow fluorescent protein (SOD1YFP) transgenic animals up to 6 mo of age. We examined 11 intrinsic electrophysiologic properties of adult ChAT-eGFP mouse MNs and classified them into four subtypes based on these parameters. The subtypes could be principally correlated with instantaneous (initial) and steady-state firing rates. We used retrograde tracing using fluorescent dye injected into fast or slow twitch lower extremity muscle with slice recordings from the fluorescent-labeled lumbar MN cell bodies to establish that fast and slow firing MNs are connected with fast and slow twitch muscle, respectively. In a G85R SOD1YFP transgenic mouse model of ALS, which becomes paralyzed by 5–6 mo, where MN cell bodies are fluorescent, enabling the same type of recording from spinal cord tissue slices, we observed that all four MN subtypes were present at 2 mo of age. At 4 mo, by which time substantial neuronal SOD1YFP aggregation and cell loss has occurred and symptoms have developed, one of the fast firing subtypes that innvervates fast twitch muscle was lost. These results begin to describe an order of the pathophysiologic events in ALS.Amyotrophic lateral sclerosis (ALS; Lou Gehrig’s disease) is a progressive and usually lethal neurodegenerative condition prominently featuring loss of motor neurons (MNs) and muscle denervation (1–3). Inherited forms of ALS, accounting for ∼10% of cases, potentially inform about disease mechanisms, including: protein folding and quality control [e.g., mutant superoxide dismutase 1 (SOD1), ubiquilin2, and VCP]; RNA binding proteins (e.g., TDP43, FUS, and HNRNPA1); or a DNA expansion (C9ORF72 hexanucleotide expansion). The clinical courses of the various heritable forms and the 90% of cases that are considered sporadic are not distinct, however, reflecting a potentially shared progressive loss of MNs and motor circuit dysfunction (4).ALS has been modeled in mice that are transgenic for a variety of mutant forms of SOD1, allowing for the study of the trajectory of the condition at various time points (5, 6). Among the studies conducted to date are a number addressing electrophysiological changes. From these studies, however, there does not appear to be a clear consensus on the changes that occur in MNs before and during the development of symptoms (7). For example, whereas research on the neuromuscular junction has revealed preferential denervation of fast twitch (type IIb) muscle fibers (8–10), the relationship of this selective susceptibility at the muscle level to pathophysiologic change in the spinal cord is not clear.A major challenge to understanding spinal cord physiology of the mouse models of ALS arises from difficulty in distinguishing the individual features of neurons in the anatomically and physiologically heterogeneous motor system. For example, the usefulness of in vivo recordings requires ensuring adequate sampling of anatomically and functionally heterogeneous spinal cord MNs. For the ex vivo alternative, slice physiology is challenging because most mouse models develop disease after 1 mo of age, a time when spinal cord tissue becomes more sensitive to ischemia (11, 12), making isolation of viable slices difficult. In addition, the spinal cord becomes heavily myelinated in the first few weeks of postnatal life (13), making visualization of individual neurons difficult. Hence, most research regarding cellular electrophysiology in mouse models of ALS has been carried out with primary cultures of embryonic (E13–14) spinal cord MNs (14) or induced pluripotent stem (iPS) cell-derived MNs (15). Although they provide a basis for further study, these models may lack the changes that occur progressively in the context of an intact spinal cord. These models may also lack the diversity of MN physiology present in the mature spinal cord.Here we studied a transgenic strain of ALS mice, G85R SOD1YFP (16), that develops motor symptoms by ∼3 mo of age, associated with progressive accumulation of aggregates in MN cell bodies (from ∼1 mo of age), attended by MN cell loss. The mice paralyze uniformly by 5–6 mo of age. We first developed, using ChAT- EGFP mice that express GFP fluorescence in MNs (17), an acute slice preparation of adult mouse spinal cord that yielded healthy MNs in animals up to and beyond 6 mo of age, readily visualized by their fluorescence, enabling whole cell patch-clamp recordings when coupled with differential interference contrast (DIC) imaging. This preparation allowed extensive characterization of normal MN electrophysiology and enabled grouping of MNs, distinguishing four firing types. We then recorded from MNs in slices from ALS animals at two time points: during the course of aggregation at 2–3 mo of age, before symptoms, and after the onset and initial progression of symptoms at 4 mo of age. At the early time, the four distinct clusters of MNs were present, albeit the fastest firing type (cluster 4) exhibited a significant hyperpolarization. At the later time point, this firing type was no longer detectable, with only the other three types observable, the fastest of which (cluster 3) was now hyperpolarized. Retrograde tracing from fast and slow twitch muscles of the lower extremity revealed that aggregates form preferentially in MN cell bodies attached to fast twitch muscle. These observations suggest a possible sequence of events in which hyperpolarization of the cluster 4 MNs, innervating fast twitch muscle, is associated with aggregate formation in these neurons, which then die, denervating fast twitch muscle.