Reliability of the American Medical Association guides' model for measuring spinal range of motion. Its implication for whole-person impairment rating

STUDY DESIGN: Repeated measures design for intra- and interrater reliability. OBJECTIVES: To determine the intra- and interrater reliability of the lumbar spine range of motion measured with a dual inclinometer, and the thoracolumbar spine range of motion measured with a long-arm goniometer, as recommended in the American Medical Association Guides. SUMMARY OF BACKGROUND DATA: The American Medical Association Guides (2nd and 4th editions) recommend using measurements of thoracolumbar and lumbar range of movement, respectively, to estimate the percentage of permanent impairment in patients with chronic low back pain. However, the reliability of this method of estimating impairment has not been determined. METHODS: In all, 34 subjects participated in the study, 21 women with a mean age of 40.1 years (SD, +/- 11.1) and 13 men with a mean age of 47.7 years (SD, +/- 12.1). Measures of thoracolumbar flexion, extension, lateral flexion, and rotation were obtained with a long-arm goniometer. Lumbar flexion, extension, and lateral flexion were measured with a dual inclinometer. Measurements were taken by two examiners on one occasion and by one examiner on two occasions approximately 1 week apart. RESULTS: The results showed poor intra- and interrater reliability for all measurements taken with both instruments. Measurement error expressed in degrees showed that measurements taken by different raters exhibited systematic as well as random differences. As a result, subjects measured by two different examiners on the same day, with either instrument, could give impairment ratings ranging between 0% and 18% of the whole person (excluding rotation), in which percentage impairment is calculated using the average range of motion and the average systematic and random error in degrees for the group for each movement (flexion, extension, and lateral flexion). CONCLUSIONS: The poor reliability of the American Medical Association Guides' spinal range of motion model can result in marked variation in the percentage of whole-body impairment. These findings have implications for compensation bodies in Australia and other countries that use the American Medical Association Guides' procedure to estimate impairment in chronic low back pain patients.     

Antiplatelet effect of amlodipine: a possible mechanism through a nitric oxide-mediated process.

The effect of amlodipine, a novel calcium channel blocker of the dihydropyridine type, on rabbit platelet aggregation, and the possible antiaggregatory mechanisms of amlodipine, especially on the nitric oxide (NO) guanosine 3',5'-cyclic monophosphate (cyclic GMP)-mediated pathway, were investigated. Other effects of amlodipine on thromboxane B2 (TXB2) formation in platelets also were examined. Amlodipine concentration-dependently inhibited rabbit platelet aggregation induced by collagen (10 microg/mL) or thrombin (0.1 U/mL) with an IC50 range of 32-69 microM. Along with this inhibition, our results also demonstrated that in the presence of L-arginine (100 IM), amlodipine (50 microM) increased nitric oxide synthetase (NOS) activity (from the resting activity of 2.05+/-0.36 to 7.11+/-0.95 pmol/mg protein/min) and NO release (by 80%), accompanied by an elevation of the cyclic GMP level (from the resting platelet level of 1.27+/-0.12 to 6.21+/-0.55 pmol/10(9) platelets) induced by collagen (10 microg/mL). However, the antiaggregatory effect of amlodipine (50 microM) could be attenuated significantly by oxyhemoglobin (5 microM), a NO scavenger, or N(G)-nitro-L-arginine methyl ester (100 microM), a specific NOS inhibitor. In addition, the TXB2 production in platelets induced by collagen or thrombin was concentration-dependently inhibited by amlodipine. Therefore, we propose that the antiaggregatory mechanisms of amlodipine might be mediated, in part, by a NO-cyclic GMP process accompanied by the inhibition of TXB2 formation in platelets.     

一叶秋碱诱导人白血病HL—60细胞凋亡

目的 研究一叶秋碱能否诱导ＨＬ－６０细胞凋亡,方法 用ＭＴＴ法检测一叶秋碱对细胞增殖影响;应用流式细胞仪检测凋亡细胞数;采用琼脂糖凝胶电泳法观测ＤＮＡ碎片,透射电镜观察凋亡的形态改变,结果：一叶秋碱５－８０ｍｇ．Ｌ＾－１能诱导ＨＬ－６０细胞凋亡,电镜观察到典型的凋亡形态学改变,电泳呈现出阶梯状条带,流式细胞仪检测到凋亡率随剂量的增高而升高,ＭＴＴ法示一叶秋碱抑制ＨＬ－６０细胞增殖,并且呈时间,剂量     

Cardiogenic shock: thrombolysis or angioplasty?

Cardiogenic shock (CGS) occurs in 3 to 20% of patients presenting with acute myocardial infarction (MI), and it generally involves dysfunction of at least 40% of the total myocardial mass. Prior to the advent of balloon angioplasty and thrombolysis, in-hospital mortality was greater than 75%. This mortality rate has been consistent in reported series despite the advent of cardiac intensive care units, vasopressor, inotropic, and vasodilator therapy. Intra-aortic balloon counterpulsation therapy provides hemodynamic improvement, and it may provide some mortality benefit when used in conjunction with appropriate revascularization. Survival studies have shown that patency of the infarct-related artery is a strong predictor of survival. No randomized trials have been completed to examine which reperfusion therapy best treats this emergent situation. Subgroup analysis of large scale, multicenter trials, although underpowered, has shown no improvement in mortality with use of thrombolytic agents, leading many to advise use of mechanical intervention. In patients who present with acute MI with contraindications to thrombolysis, primary angioplasty is the treatment of choice. At selected centers, primary angioplasty is comparable to or better than thrombolytic therapy for patients presenting with acute MI, with or without CGS. Studies examining angioplasty in patients with CGS have shown high procedural success rates (75%) and reduced in-hospital mortality (44%), particularly in those patients with successful revascularization. Emergency bypass surgery may improve survival, but it is costly, unavailable to many, and often leads to excessive delays in therapy. If available, we believe that primary angioplasty is the treatment of choice for patients with CGS.     

Experimental tests of three-dimensional model of urinary concentrating mechanism.

Recently, a new model of the urinary concentrating process has been proposed that takes into account the three-dimensional architecture of the renal medulla. Under the assumptions of the model, computer simulations predicted significant axial osmolality gradients in the inner medulla without active transport by the inner medullary loop of Henle. Two of the model assumptions (which constitute hypotheses for this study) were: (1) the osmotic water permeability of the initial part of the inner medullary collecting duct (initial IMCD) is very low even in the presence of vasopressin; and (2) there is significant lateral separation of structures such that thin descending limbs are far from the collecting ducts at the same inner medullary level. The first hypothesis was addressed by perfusing rat initial IMCD segments in vitro and measuring osmotic water permeability. With the osmotic gradient oriented as predicted by the model (lumen greater than bath), vasopressin increased the osmotic water permeability from 286 to 852 microns/s. Three additional series of experiments confirmed the high water permeability in the presence of vasopressin. The second hypothesis was addressed by morphometric analysis of histologic cross-sections of the rat renal medulla. Mean distances of descending limbs to the nearest adjacent collecting duct were very small throughout the inner medulla (less than 6 microns) and substantially less than in the outer medulla (28 microns). It was concluded that the data are inconsistent with both hypotheses and therefore do not support the feasibility of the "three-dimensional" model of the renal inner medulla. The axial distributions of loops of Henle and collecting ducts in the rat renal medulla are also reported.     

Role of macrophages in onion-bulb formation in localized hypertrophic mononeuritis (LHM).

A unique pathogenetic process for onion-bulb (Ob) formation is disclosed with disclosed with immunohistochemistry and electron microscopy. Biopsy of a swollen segment of tibial nerve from a 42 year-old white female histologically demonstrated diffuse and angiocentric lymphocytic infiltrate in both endo- and perineurium with occasional lymphofollicular formation. Extensive Ob formation of nerve fibers was most striking with or without associated lymphocytes. Axis-cylinders were intact in the majority of Ob. Immunocytochemically, Ob are composed of alternately laminated leaflets of Schwann cells (S100+) and mononuclear macrophage (HAM56+/LeuMl+/Muramidase+) processes but no perineurial (EMA+) cells. Immunohistochemical evidence of antigen presentation (HLA-DR/LN3+/Ia+) was confined to macrophages. Electron microscopy insinuates that intricate interactions between macrophages and Schwann cells exists. Putative inhibition of remyelination along with proliferation of Schwann cells most probably is secondary to the effects of macrophages secretory products. No direct participation of B or T lymphocytes was detected in Ob. Thus, modified macrophages may emit a factor for concomitantly promoting proliferation of Schwann cells and an enzyme for myelin breakdown. In addition, only a few macrophages could be detected in some Ob and could be easily overlooked or misinterpreted as "vacuolated fibroblasts", if no immunohistochemical correlation is made, as modified macrophages making the external leaflets of Ob are more vacuolated.     

Tumorigenicity of 7, 12-dimethylbenz[a]anthracene, its hydroxy-methylated derivatives and selected dihydrodiols in the newborn mouse

The newborn mouse lung adenoma model has been shown to be asensitive test for studying the tumor-igenicity of bay regiondiol epoxides and their precursor dihydrodiols. When a totaldose of 28 nmol of 7, 12-dimethylbenz[a]anthracene (DMBA) orits derivatives was injected i.p. into the preweaning mice,it was found that the 3, 4-dihydrodiols of both DMBA and 7-hy-droxymethyl-12-methylbenz[a]anthracenecaused 13.3 and 4.1 times more lung adenomas than DMBA, respectively.The mice treated with the 5, 6- and 8, 9-dihydro-diols of DMBA,7-hydroxymethyl-12-methylbenz[a]-anthracene and its 5, 6- 8,9-and 10,11-dihydrodiols, 7-methyl-12-hydroxymethylbenz[a]an-thraceneand 7,12-dihydroxymethylbenz[a]anthracene developed a levelof lung adenomas/mouse less than Mold higher than that foundin the DMSO-treated control group. Liver tumors also developedin some of the mice. The percentage of mice with liver tumorsalso indicated that the 3, 4-dihydrodiols of both DMBA and 7-hydroxymethyl-12-methylbenz[a]anthracenewere more tumorigenic than DMBA itself. These data indicatethat the 3, 4-dihydrodiols of both DMBA and its 7-hydroxymethylderivative may be proximate carcinogenic metabolites of DMBAin the newborn mouse.     

Effects of support group intervention in postnatally distressed women. A controlled study in Taiwan

Objective: The symptoms of depression experienced by women during the postnatal period may have profound effects on the lifelong health of both the mother and the child. In this randomized controlled study, we systematically evaluated the effects of weekly supportive group meetings for women with postnatal distress. Methods: Sixty postnatally distressed women were randomly assigned to support (n=30) and control (n=30) groups. Women assigned to the support group participated in four supportive group sessions that comprised discussions concerning transition to motherhood, postnatal stress management, communication skills, and life planning. Results: Subjects who attended the support sessions had significantly decreased scores on the Beck Depression Inventory (BDI) and the Perceived Stress Scale (PSS), and significantly increased scores on the Interpersonal Support Evaluation List (ISEL) as evaluated at the end of the fourth weekly session. In contrast, no significant changes were observed in the control group during this period. Conclusion: This is the first controlled study to provide evidence that participation in support groups for postnatally distressed women provides quantifiable psychosocial benefits.     

Unexpected recurrent seizures following repeated spinal injections of tetracaine--a case report

A 36-year-old male patient was scheduled to undergo ureteroscopic lithotomy because of left ureteral stone under spinal anesthesia. After receiving a renewed spinal anesthesia with 8 mg tetracaine to compensate for the first attempt (with 10 mg tetracaine), which proved to be a failure, he was soon seized with episodic seizure attacks. Central nervous system toxicity of the local anesthetic might be the cause of the seizure. We brought forward this case for discussion for warning that the possibility of systemic toxicity of local anesthetic might exist despite a seemingly undisputable spinal anesthesia.     

Effects of intermittent exposure to aflatoxin B1 on DNA and RNA adduct formation in rat liver: dose-response and temporal patterns.

We studied the effects of intermittent exposure to aflatoxin B1 (AFB1) on hepatic DNA and RNA adduct formation. Fisher-344 male rats were fed 0.01, 0.04, 0.4, or 1.6 ppm of AFB1 intermittently for 8, 12, 16, and 20 weeks, alternating with 4 weeks of dosing and 4 weeks of rest. Other groups of rats were fed 1.6 ppm of AFB1 continuously for 4, 8, 12, and 16 weeks. Control rats received AFB1-free NIH-31 meal diet. AFB1-DNA and -RNA adducts were measured by HPLC with fluorescence detection. The data are presented as total DNA or RNA adducts. The DNA and RNA adduct levels increased or decreased depending on the cycles of dosing and rest. Rats removed from treatment 1 month after 1 or 2 dosing cycles (8 and 16 weeks of intermittent exposure) showed approximately a twofold decrease in DNA adduct levels and a two- to elevenfold decrease in RNA adduct levels compared with rats euthanized immediately after the last dosing cycle (12 and 20 weeks of intermittent exposure). Our data indicate that DNA and RNA adducts increased linearly, from 0.01 ppm to 1.6 ppm of AFB1 after 12 and 20 weeks of intermittent treatment. A linear dose response was also apparent for DNA but not for RNA adducts after 8 and 16 weeks of treatment. As biomarkers of exposure, AFB1-RNA adducts were three to nine times more sensitive than AFB1-DNA adducts but showed greater variability. These results suggest that binding of AFB1 to hepatic DNA is a linear function of the dose, regardless of the way this is administered. The dose-response relationship for RNA adducts depends on the length of the no-dosing cycles and on the turnover rate of RNA.