Lumbar fractures in adult blunt trauma: axial and single-slice helical abdominal and pelvic computed tomographic scans versus portable plain films

BACKGROUND: Our hypothesis was that abdominal and pelvic computed tomographic (AP-CT) scans are equivalent to portable two-view plain films in detecting lumbar spine fractures in adults. Since many trauma patients often undergo AP-CT scanning to evaluate for possible intra-abdominal injuries, using the AP-CT scan to screen for lumbar fractures could make the trauma evaluation process more efficient. METHODS: The institutional trauma registry at a Level I trauma center was used to identify all blunt lumbar fractures during a 6-year period. Medical records were reviewed. RESULTS: A total of 7,216 adult blunt trauma patients were evaluated, and 115 patients were identified as having a lumbar fracture, for an incidence rate of 1.6%. Missed fracture rates were high for both AP-CT scans (23.2%, 13 of 56) and portable two-view films (12.7%, 14 of 110, = 0.08). Fifty-two patients had both AP-CT scans and plain films. In this group, AP-CT scans missed 23.1% (12 of 52) of the lumbar fractures and plain films missed 15.4% (8 of 52). However, the combination of the two diagnostic methods did not miss any fractures (0 of 52). The missed fractures required surgery or brace in 50% (7 of 14) patients who had fractures missed by plain films and 46% (6 of 13) patients whose fractures were missed by AP-CT scanning. CONCLUSION: Both AP-CT scans and plain films failed to diagnose significant lumbar fractures that required therapy. When screening for lumbar fractures, obtaining both AP-CT scans and portable two-view plain films may decrease missed lumbar fractures in blunt adult trauma.     

How to simplify the CT diagnosis of Le Fort fractures

OBJECTIVE: The numerous components seen in the Le Fort fractures make classification difficult. Our objective is to simplify the task of classifying Le Fort fractures. CONCLUSION: Each of the Le Fort fractures has at least one unique component that is easily recognizable: I, the anterolateral margin of the nasal fossa; II, the inferior orbital rim; and III, the zygomatic arch. Classification of the Le Fort fractures is simplified by using these unique components to establish a tentative classification that is then confirmed.     

Estimated glomerular filtration rate in sickle cell anemia is associated with polymorphisms of bone morphogenetic protein receptor 1B

Renal disease is common in sickle cell anemia. In this exploratory work, we used data from a longitudinal study of the natural history of sickle cell disease to examine the hypothesis that polymorphisms (SNPs) in selected candidate genes are associated with glomerular filtration rate (GFR). DNA samples and clinical and laboratory data were available for 1,140 patients with sickle cell anemia. GFR was estimated using the Cockcroft-Gault and Schwartz formulas for adults and children, respectively. We examined approximately 175 haplotype tagging (ht) SNPs in about 70 genes of the TGFbeta/BMP pathway for their association with GFR using linear regression. Four SNPs in BMPR1B, a bone morphogenetic protein (BMP) receptor gene, yielded statistically significant associations (P values ranging from 0.015 to 0.046). Three haplotypes in this gene were also associated with GFR. The TGF-beta/BMP pathway has been associated with the development of diabetic nephropathy, which has some features in common with sickle cell nephropathy. Our results suggest that, as with other subphenotypes of sickle cell disease, renal function may be genetically modulated.     

速度滑冰与短道速度滑冰运动员身体功能评定

目的:总结速度滑冰与短道速度滑冰运动员各项生理生化指标,开发应用生理生化指标对身体功能进行评定,为科学训练提供参考依据。方法:分析速度滑冰与短道速度滑冰项目特点,并根据其特点制定了各项生理生化指标的参考值。结果:速度滑冰与短道速度滑冰均有周期性耐力性项目特点,要求运动员必须具备较强的无氧代谢能力,尤其是抗乳酸能力,可用4mmol/L做无氧阈训练监控指标。血尿素参考值4￣7mmol/L,功能下降或训练量大时增高。血清肌酸激酶强度训练时可高达16.67μkat/L以上。血红蛋白参考值为男120￣160g/L,女110￣150g/L。免疫指标和内分泌指标均应定期监测,为提供身体功能信息有重要意义。结论:可用血乳酸系统监控和评估有氧与无氧耐力水平,运动员身体功能评定是科学化训练重要保证,是科学训练的重要部分。     

Thrombosis risk and survival in cancer patients with elevated C‐reactive protein

Summary. Background: The incidence of venous thromboembolism (VTE) is increased among cancer patients. Objective: We assessed serum levels of C‐reactive protein (CRP) in order to study their prognostic significance for VTE and survival in the prospective observational Cancer and Thrombosis Study (CATS). Patients and methods: This study includes patients with recently diagnosed cancer or progression of disease after remission. Occurrence of VTE and information on the patients’ anti‐cancer‐treatment are recorded. Observation ends with occurrence of objectively confirmed VTE, death or after 2 years. CRP levels were determined by an immunonephelometric method. Results: We included 705 consecutive patients with solid tumors. During the observation period, VTE occurred in 43 (6.1%) patients and 413 (58.6%) died. The cumulative probability of VTE was 6.6% after 1 year. In univariate analysis, CRP (as metric variable, per double increase) was associated with VTE [hazard ratio (HR) 1.2, 95% confidence interval (CI) 1.1–1.3 P = 0.048]. However, in multivariable analysis including chemotherapy, surgery and radiotherapy, metastasis, cancer‐site and sP‐selectin the association with VTE (HR 1.0, 95% CI 0.9–1.2 P = 0.932) was no longer observed. CRP was clearly associated with worse survival probability with a HR of 1.3 (95% CI 1.2–1.3, P < 0.0001) in multivariable analysis. The cumulative survival after 12 months was 43% in patients with CRP above the 75th percentile (1.8 mg dL^?1) and 82% in those below the 75th percentile. Conclusions: In cancer patients elevated CRP was not independently associated with VTE. CRP was significantly associated with worse survival.     

Economic realities associated with diabetes care: opportunities to expand delivery of physical therapist services to a vulnerable population

Each year, more Americans are newly diagnosed with type 2 diabetes mellitus. The costs for managing this disease are high, and the cascade of problems associated with poorly controlled diabetes is significant. At the same time, the number of uninsured or underinsured Americans is growing. This article describes current trends in health insurance availability and coverage for the growing number of people with diabetes and addresses the direct costs associated with treating this disease. The economic burden of health care for people with diabetes continues to escalate. Payers and employers are interested in decreasing their direct and indirect costs, improving profit margins, decreasing employee absenteeism, and increasing employee productivity. For physical therapists to recognize existing or new opportunities to participate in the management of this costly disease, it is critical that they understand how employees, payers, and employers are responding to the changing market forces affecting health insurance.     

INAUGURAL ARTICLE by a Recently Elected Academy Member:Autosis is a Na+,K+-ATPase–regulated form of cell death triggered by autophagy-inducing peptides,starvation, and hypoxia–ischemia

A long-standing controversy is whether autophagy is a bona fide cause of mammalian cell death. We used a cell-penetrating autophagy-inducing peptide, Tat-Beclin 1, derived from the autophagy protein Beclin 1, to investigate whether high levels of autophagy result in cell death by autophagy. Here we show that Tat-Beclin 1 induces dose-dependent death that is blocked by pharmacological or genetic inhibition of autophagy, but not of apoptosis or necroptosis. This death, termed “autosis,” has unique morphological features, including increased autophagosomes/autolysosomes and nuclear convolution at early stages, and focal swelling of the perinuclear space at late stages. We also observed autotic death in cells during stress conditions, including in a subpopulation of nutrient-starved cells in vitro and in hippocampal neurons of neonatal rats subjected to cerebral hypoxia–ischemia in vivo. A chemical screen of ∼5,000 known bioactive compounds revealed that cardiac glycosides, antagonists of Na⁺,K⁺-ATPase, inhibit autotic cell death in vitro and in vivo. Furthermore, genetic knockdown of the Na⁺,K⁺-ATPase α1 subunit blocks peptide and starvation-induced autosis in vitro. Thus, we have identified a unique form of autophagy-dependent cell death, a Food and Drug Administration-approved class of compounds that inhibit such death, and a crucial role for Na⁺,K⁺-ATPase in its regulation. These findings have implications for understanding how cells die during certain stress conditions and how such cell death might be prevented.The lysosomal degradation pathway of autophagy plays a crucial role in enabling eukaryotic cells to adapt to environmental stress, especially nutrient deprivation (1). The core autophagy machinery was discovered in a genetic screen in yeast for genes essential for survival during starvation, and gene knockout or knockdown studies in diverse model organisms provide strong evidence for a conserved prosurvival function of autophagy during starvation (1). This prosurvival function of autophagy results from its ability to mobilize intracellular energy resources to meet the demand for metabolic substrates when external nutrient supplies are limited.In contrast to this well-accepted, prosurvival function of autophagy, there has been much debate as to whether autophagy—especially at high levels—also functions as a mode of cell death (2). Historically, based on morphological criteria, three types of programmed cell death have been defined: type I apoptotic cell death; type II autophagic cell death; and type III, which includes necrosis and cytoplasmic cell death (3). Autophagic cell death was originally defined as a type of cell death that occurs without chromatin condensation and is accompanied by large-scale autophagic vacuolization of the cytoplasm. This form of cell death, first described in the 1960s, has been observed ultrastructurally in tissues where developmental programs (e.g., insect metamorphosis) or homeostatic processes in adulthood (e.g., mammary involution following lactation or prostate involution following castration) require massive cell elimination (4–6). Autophagic cell death has also been described in diseased tissues and in cultured mammalian cells treated with chemotherapeutic agents or other toxic compounds (4–6).The term “autophagic cell death” has been controversial, because it has been applied to scenarios where evidence is lacking for a causative role of autophagy in cell death (i.e., there is cell death with autophagy but not by autophagy). However, using more stringent criteria to define autophagic cell death, several studies in the past decade have shown that autophagy genes are essential for cell death in certain contexts. This includes cases of tissue involution in invertebrate development as well as in cultured mammalian cells lacking intact apoptosis pathways (6, 7). In apoptosis-competent cells, high levels of autophagy can also lead to autophagy gene-dependent, caspase-independent cell death (8–10). In neonatal mice, neuron-specific deletion of Atg7 protects against cerebral hypoxia–ischemia-induced hippocampal neuron death (11), and in adult rats, shRNA targeting beclin 1 decreases neuronal death in the thalamus that occurs secondary to cortical infarction (12).Although such studies provide genetic support for autophagy as a bona fide mode of cell death, the nature of autophagic cell death that occurs in mammalian cells and tissues in response to physiological/pathophysiological stimuli remains poorly defined. It is unclear whether cells that die by autophagy have unique morphological features or a unique death machinery. The only morphological feature that has been linked to autophagic cell death—autophagic vacuolization—may be observed in cells undergoing apoptotic or necrotic cell death, and no proteins, aside from the core autophagy proteins, have been shown to be required for autophagic cell death.Here we identify a form of autophagic cell death, autosis, which has unique morphological features; depends on the cellular Na⁺,K⁺-ATPase; and occurs during treatment with autophagy-inducing peptides, starvation, and cerebral hypoxia–ischemia.     

Detection of Mycobacterium tuberculosis in bronchoalveolar lavage from patients with sputum smear-negative pulmonary tuberculosis using a polymerase chain reaction assay

Abstract The objective of this study was to evaluate the utility of a polymerase chain reaction (PCR) assay in detecting Mycobacterium tuberculosis in bronchoalveolar lavage (BAL) specimens of patients suspected of having active pulmonary tuberculosis (TB) but who were sputum smear-negative. Patients undergoing investigation for suspected pulmonary TB at the University Hospital, Kuala Lumpur, and who were sputum smear-negative underwent fibreoptic bronchoscopy and BAL. One portion of each lavage specimen was submitted for smear examination for acid-fast bacilli and mycobacterial culture and the other portion assayed by PCR for the presence of a 562-base pair DNA segment belonging to the insertion sequence IS986, unique to the M. tuberculosis complex. As controls, lavage specimens from patients with other lung lesions were also similarly tested. The PCR assay gave a positivity rate of 80.9% (55 of 68) compared with 8.8% of smear examination and 7.4% of culture for detecting M. tuberculosis in BAL specimens. The assay was positive in two of 45 BAL specimens from 35 control subjects. The PCR assay was more sensitive than smear and culture in detecting M. tuberculosis in BAL specimens of patients with sputum smear-negative pulmonary TB.     

Histology as a diagnostic tool for intestinal isosporiasis in immunocompromised patients

Isospora belli is an opportunistic protozoan causing wasting diarrhea especially in patients with an immunocompromised status. Diagnosis is usually established by demonstrating the oocyst of the organism on stool examination, which however can often be inconclusive. Serological tests for isosporiasis are currently not available. In such a scenario, biopsy often provides evidence for a confirmatory diagnosis. We describe two such cases, in which intestinal biopsy was the only diagnostic evidence of isosporiasis as the cause for chronic diarrhea.