Kihoku hospital

BACKGROUND: In patients with hepatocellular carcinoma (hepatoma), the rate of recurrent and second primary hepatomas is high despite surgical resection and percutaneous ethanol-injection therapy. We developed an acyclic retinoid, polyprenoic acid, that inhibits hepatocarcinogenesis in the laboratory and induces differentiation and apoptosis in cell lines derived from human hepatoma. In a randomized, controlled study, we tested whether the compound reduced the incidence of recurrent and second primary hepatomas after curative treatment. METHODS: We prospectively studied 89 patients who were free of disease after surgical resection of a primary hepatoma or the percutaneous injection of ethanol. We randomly assigned the patients to receive either polyprenoic acid (600 mg daily) or placebo for 12 months. We studied the remnant liver by ultrasonography every three months after randomization. The primary end point of the study was the appearance of a histologically confirmed recurrent or new hepatoma. RESULTS: Treatment with polyprenoic acid significantly reduced the incidence of recurrent or new hepatomas. After a median follow-up of 38 months, 12 patients in the polyprenoic acid group (27 percent) had recurrent or new hepatomas as compared with 22 patients in the placebo group (49 percent, P = 0.04). The most striking difference was in the groups that had second primary hepatomas--7 in the group receiving polyprenoic acid as compared with 20 in the placebo group (P = 0.04 by the log-rank test). Cox proportional-hazards analysis demonstrated that as an independent factor, polyprenoic acid reduced the occurrence of second primary hepatomas (adjusted relative risk, 0.31; 95 percent confidence interval, 0.12 to 0.78). CONCLUSIONS: Oral polyprenoic acid prevents second primary hepatomas after surgical resection of the original tumor or the percutaneous injection of ethanol.

Retrospective analysis has shown that activating mutations in exons 18-21 of the epidermal growth factor receptor (EGFR) gene are a predictor of response to gefitinib. We conducted a phase II trial to evaluate the efficacy and safety of gefitinib as first-line therapy for advanced non-small cell lung cancer (NSCLC) with EGFR mutations. Patients with stage IIIB or IV chemotherapy-naïve NSCLC with EGFR mutation were treated with 250 mg gefitinib daily. For mutational analysis, DNA was extracted from paraffin-embedded tissues and EGFR mutations were analysed by direct sequence of PCR products. Twenty (24%) of the 82 patients analysed had EGFR mutations (deletions in or near E746-A750, n=16; L858R, n=4). Sixteen patients were enrolled and treated with gefitinib. Twelve patients had objective response and response rate was 75% (95% CI, 48-93%). After a median follow-up of 12.7 months (range, 3.1-16.8 months), 10 patients demonstrated disease progression, with median progression-free survival of 8.9 months (95% CI, 6.7-11.1 months). The median overall survival time has not yet been reached. Most of the toxicities were mild. This study showed that gefitinib is very active and well tolerated as first-line therapy for advanced NSCLC with EGFR mutations.

BACKGROUND: In a controlled and double-blind study, the authors tested the hypothesis that preoperative insertion of intradermal needles at acupoints 2.5 cm from the spinal vertebrae (bladder meridian) provide satisfactory postoperative analgesia. METHODS: The authors enrolled patients scheduled for elective upper and lower abdominal surgery. Before anesthesia, patients undergoing each type of surgery were randomly assigned to one of two groups: acupuncture (n = 50 and n = 39 for upper and lower abdominal surgery, respectively) or control (n = 48 and n = 38 for upper and lower abdominal surgery, respectively). In the acupuncture group, intradermal needles were inserted to the left and right of bladder meridian 18-24 and 20-26 in upper and lower abdominal surgery before induction of anesthesia, respectively. Postoperative analgesia was maintained with epidural morphine and bolus doses of intravenous morphine. Consumption of intravenous morphine was recorded. Incisional pain at rest and during coughing and deep visceral pain were recorded during recovery and for 4 days thereafter on a four-point verbal rating scale. We also evaluated time-dependent changes in plasma concentrations of cortisol and catecholamines. RESULTS: Starting from the recovery room, intradermal acupuncture increased the fraction of patients with good pain relief as compared with the control (P < 0.05). Consumption of supplemental intravenous morphine was reduced 50%, and the incidence of postoperative nausea was reduced 20-30% in the acupuncture patients who had undergone either upper or lower abdominal surgery (P < 0.01). Plasma cortisol and epinephrine concentrations were reduced 30-50% in the acupuncture group during recovery and on the first postoperative day (P < 0.01). CONCLUSION: Preoperative insertion of intradermal needles reduces postoperative pain, the analgesic requirement, and opioid-related side effects after both upper and lower abdominal surgery. Acupuncture analgesia also reduces the activation of the sympathoadrenal system that normally accompanies surgery.

In this communication, we demonstrate the sequential expression of endogenous molecules, including immediate early genes (IEGs), cytokines, neurotrophins, and neurotrophin receptors in the injured spinal cord. In the acute phase, expression of IEGs and cytokines mRNAs were rapidly upregulated within 1 h in nonneuronal cells in the lesioned sites and the surrounding spinal white and gray matter. Maximal expression was observed at 1 h for c-fos and TNF-alpha mRNAs, at 3 h for c-jun and IL-6 mRNAs, and at 6 h for IL-1 beta mRNA, and these signals were virtually nondetectable after 6-12 h from the onset of the injury. Some of these genes products may promote the degeneration of damaged cells and tissues, while others may be involved in the subsequent repair processes. In the subacute phase, expression of NGF, BDNF, NT-3, p75LNGFR and Trk B mRNAs began to increase in the nonneuronal cells and neuronal cells from 6 h, and peaked at 24-72 h in the area where expression of mRNAs for IEGs and cytokines overlapped. Signals for IL-6 mRNA were also observed in motoneurons at 24-72 h after the injury, with the suggestion that these molecules may be involved in promoting axonal sprouting in the injured spinal cord. Of further interest was the finding that this upregulation of IL-1 beta, BDNF, and NT-3 mRNAs in injured spinal cord was attenuated by treatment with high dose glucocorticoids, with the suggestion that the downregulation of BDNF and NT-3 might be disadvantageous to survival and axonal sprouting of spinal neurons.

STUDY DESIGN: A prospective, randomized, and double-blind study comparing high-dose methylprednisolone sodium succinate (MPSS) with placebo, in the treatment of patients with acute cervical spinal cord injury. OBJECTIVES: To evaluate the complications of high-dose MPSS in patients with acute cervical spinal cord injury when administered within 8 hours of injury. SUMMARY OF BACKGROUND DATA: High-dose therapy with MPSS has been demonstrated to improve the recovery of motor function in patients with acute cervical spinal cord injury. However, little is known about the follow-up complications. METHODS: Forty-six patients, 42 men and 4 women (mean age, 60.6 years; range, 18-84), were included in the study: 23 in the MPSS group and 23 in the placebo group. They were treated without surgery for spinal cord injury in the cervical spine, and were enrolled in the trial if a diagnosis had been made and treatment had begun within 8 hours. Complications of high-dose therapy with MPSS were compared with placebo treatment throughout the study period and up to 2 months after injury. RESULTS: The MPSS group had 13 patients (56.5%) with complications, whereas the placebo group had 8 (34.8%). The difference between the two groups was not statistically significant (P = 0.139). There were eight instances of pulmonary complication with MPSS (34.8%) and one instance (4.34%) with placebo (P = 0.009). There were four instances of gastrointestinal complication (17.4%) with MPSS and none with placebo (P = 0.036). Pulmonary (complications were more prevalent in patients aged more than 60 years (P = 0.029). CONCLUSION: Aged patients with cervical spinal injury may be more likely to have pulmonary side effects (P = 0.029) after high-dose therapy with MPSS and thus deserve special care.

To investigate the pathogenesis of hypertrophy of the ligamentum flavum, 45 cases of lumbar canal stenosis were evaluated by computed tomography scan and pathologic and immunohistochemical studies. The ligamentum flavum along with the medial one-third of the superior facet was obtained en bloc to include the enthesis. Statistically significant differences in transverse area and thickness of the ligamentum flavum were evident compared to the control group (P < 0.01). Pathogenesis of the hypertrophied ligamentum flavum was classified into three major groups: 1) fibrocartilage change due to proliferation of type II collagen, 2) ossification, and 3) calcium crystal deposition. It is stressed that marked proliferation of Type II collagen from the enthesis to the ligament side was revealed in the capsular portion of the hypertrophied ligament.

Human 3alpha-hydroxysteroid dehydrogenase exists in four isoforms, which belong to the aldo-keto reductase (AKR) superfamily and are named AKR1C1-AKR1C4. The properties of AKR1C3 have not been fully characterized compared to the other isoforms. In addition, a cDNA that shows more than 99% homology with AKR1C3 cDNA has been cloned from human myeloblasts. We have here expressed and purified a recombinant enzyme (designated as DBDH) from this cDNA. DBDH oxidized xenobiotic alicyclic alcohols and 3alpha- or 17beta-hydroxy-5beta-androstanes, and catalyzed the reversible conversion between prostaglandin D2 and 9alpha,11beta-prostaglandin F2 more efficiently than that of 3alpha- or 17beta-hydroxysteroids:the respective Km values were 0.6 and 6.8 microM, and kcat/Km values were about 1,000 min-1.mM-1. Anti-inflammatory drugs highly inhibited the enzyme. The recombinant AKR1C3 prepared by site-directed mutagenesis of DBDH also showed the same properties as the wild-type DBDH. Analyses of expression of mRNAs for DBDH and AKR1C3 by reverse transcription-PCR indicated that only one mRNA species for DBDH is expressed in 33 human specimens of liver, kidney, lung, brain, heart, spleen, adrenal gland, small intestine, placenta, prostate, and testis. These results suggest that AKR1C3 acts as prostaglandin D2 11-ketoreductase, and that its principal gene in the human has a coding region represented by DBDH cDNA.

Since 1986 we have performed expansive laminoplasty with reattachment of the spinous processes and extensor musculature in cases of cervical myelopathy, to avoid the late postoperative complications of extensive laminectomy. The operative procedure and results are given in detail. Forty cases (24 men, 16 women) were followed for a mean of 28 months. Postoperative results were satisfactory, with no major complications according to the evaluation criteria of the Japanese Orthopaedic Association. No instability or malalignment was seen on postoperative radiographs.

Increased production of calcitonin gene-related peptide (CGRP) in sensory neurons is implicated in inflammatory pain. The inflammatory site is acidic due to proton release from infiltrating inflammatory cells. Acid activation of peripheral nociceptors relays pain signals to the CNS. Here, we examined whether acid activated the transient receptor potential vanilloid subtype 1 (Trpv1), a widely recognized acid-sensing nociceptor and subsequently increased CGRP expression. Chemically induced inflammation was associated with thermal hyperalgesia and increased CGRP expression in dorsal root ganglion (DRG) in rats. In organ cultures of DRG, acid (pH 5.5) elevated CGRP expression and the selective Trpv1 antagonist 5'-Iodoresiniferatoxin decreased it. Trpv1-deficient DRG showed reduced CGRP increase by acid. Of note, many of CGRP/Trpv1-positive DRG neurons exhibited the phosphorylation of cAMP response element-binding protein (CREB), a nociceptive transcription factor. Knockdown of CREB by small interfering RNA or a dominant-negative form of CREB diminished acid-elevated CGRP expression. Acid elevated the transcriptional activity of CREB, which in turn stimulated CGRP gene promoter activity. These effects were inhibited by a Ca(2+)/calmodulin-dependent protein kinase (CaMK) inhibitor KN-93. In conclusion, our results suggest that inflammatory acidic environments activate Trpv1, leading to an up-regulation of CGRP expression via CaMK-CREB cascade, a series of events that may be associated with inflammatory pain.

The pathophysiologic mechanisms of painful radiculopathy caused by a herniated intervertebral disc remain unknown. This study sought to determine whether the autologous intervertebral disc produces pain related behavior and whether phospholipase A2 and nitric oxide are involved in the pathophysiologic mechanism producing the behavior. A rat model, in which autologous intervertebral discs were implanted on the nerve root in the lumbar spine, was used to measure hyperalgesia, which is a pain related behavior in the rat. In this experimental model, autologous nucleus pulposus and anulus fibrosus transplanted to lumbar nerve roots produced mechanical and thermal hyperalgesia, respectively. Epidural injection of a selective inhibitor for phospholipase A2 resulted in the disappearance of hypersensitivity to noxious mechanical stimuli. Thermal hyperalgesia produced by application of the anulus fibrosus was abated and abolished by epidural injections of saline and one of the inhibitors for nitric oxide synthase, respectively. The authors suggest that chemical mediators such as phospholipase A2 and nitric oxide, induced by extruded or sequestrated intervertebral discs, are involved in the pathophysiologic mechanisms of painful radiculopathy in lumbar disc herniations. This study may be useful in attempting to develop new medical approaches for treatments of lumbar disc herniation.

OBJECTIVE: To test the hypothesis that myocardium specific proteins may be useful markers for evaluating the severity of congestive heart failure. METHODS: Serum concentrations of myosin light chain I (MLC-I), heart fatty acid binding protein (H-FABP), creatine kinase isoenzyme MB (CK-MB), and troponin T (TnT) and plasma concentrations of brain natriuretic peptide (BNP) were determined in 48 patients with acute deterioration of congestive heart failure, both before and after effective treatment. RESULTS: Before treatment, MLC-I (mean (SEM) 3.2 (2.2) microg/l), H-FABP (9.0 (3.5) microg/l), TnT (30 (21) ng/l), and BNP (761 (303) ng/l) were higher than the normal reference range, and concentrations of CK-MB (5.4 (2.9) microg/l) were near normal. Treatment of congestive heart failure with conventional medication significantly decreased the concentrations of MLC-I (1.2 (0.3) microg/l, p < 0.0001), H-FABP (6.0 (2.0) microg/l, p < 0.0001), CK-MB (2.9 (1.5) microg/l, p < 0.0001), TnT (9 (1) ng/l, p < 0.001), and BNP (156 (118) ng/l, p < 0.0001). The decreases in H-FABP and CK-MB concentrations after treatment correlated with the decrease in BNP concentrations (p < 0.05). The absolute concentrations of MLC-I, H-FABP, CK-MB, and TnT correlated positively with those of BNP (p < 0.01). CONCLUSIONS: These findings suggest that MLC-I, H-FABP, CK-MB, and TnT may be used as reliable markers for the evaluation of the severity of congestive heart failure.

STUDY DESIGN: The authors retrospectively determined the prevalence of neck and shoulder symptoms (axial symptoms) after expansive laminoplasty with reattachment of spinous process and extensor musculature in patients with cervical myelopathy. OBJECTIVES: To determine the prevalence of both preoperative and postoperative axial symptoms of expansive laminoplasty when they occur after expansive laminoplasty. SUMMARY OF BACKGROUND DATA: Several clinical reports have noted that laminoplasty for cervical myelopathy produces positive clinical outcomes. However, recent reports have pointed out that complications from laminoplasty, such as axial symptoms, may be severe enough to interfere with daily activities. METHODS: The authors used a modified spinous process-splitting laminoplasty, which involved reattaching the spinous process with extensor musculature after enlarging the spinal canal by use of the French window method. Postoperative axial symptoms were investigated in 173 of 214 patients (80.1%) who underwent expansive laminoplasty between January 1989 and December 1998. The patients included 121 men and 52 women, and their average age was 61.5 years. The presence or absence and grade of axial symptoms before and after laminoplasty were investigated. The severity and duration of complications were also recorded, along with differences between age, sex, spinal alignment, and cervical diseases. RESULTS: Neck and/or shoulder stiffness worsened in 15% of the patients and declined in 21%. Neck pain worsened in 10% of the patients and improved in 11%. Neck and/or shoulder stiffness worse than moderate was recognized in 14.4% of the patients. Neck pain worse than moderate was recognized in 5% of the patients. In the 137 patients who had no axial pain before surgery, only 13 patients experienced such symptoms after surgery, and in most cases these symptoms were minimal. In only 1 case, significant postoperative neck pain arose de novo as a result of this surgery. In 88 patients who had no neck and/or shoulder stiffness before surgery, only 16 patients experienced such symptoms after surgery, and in most cases these were minimal. A similar pattern held true for each of the other grades of preoperative axial symptoms. The recovery rate score (Japanese Orthopedic Association) was 47.5 +/- 32.3 in the patients whose axial symptoms were worse than moderate and 60 +/- 28.9 in patients whose axial symptoms were less than mild. This difference was significant (P < 0.05). CONCLUSION: Laminoplasty is an appropriate operation for cervical spondylotic myelopathy and did not, in this study, seem to have any significant influence on the development or resolution of axial symptoms.

STUDY DESIGN: in vivo analysis in an immature porcine model. OBJECTIVE: to evaluate the effect of intraoperative tensioning of an anterolateral flexible spinal tether on growth modulation manifested as deformity creation, disc response, spinal motion, and screw fixation using radiographs, computed tomography, magnetic resonance imaging, biomechanical testing, and histology. SUMMARY OF BACKGROUND DATA: spinal growth modulation using an anterolateral flexible tether has been proposed as a nonfusion surgical deformity correction strategy for idiopathic scoliosis and has been successfully demonstrated in a porcine model to create spinal deformity while maintaining disc viability. METHODS: twelve 7-month-old mini-pigs were instrumented with a screw-staple and polyethylene tether construct over 4 consecutive thoracic vertebrae (T8-T11). Intraoperative tensioning of the tether (250 N) was performed in alternate pigs (Pretensioned and Untensioned groups, n = 6 per group). Screws were coated with hydroxyapatite in half of the animals in each surgical group. Preoperative, postoperative, and monthly radiographs were evaluated, comparing deformity creation, vertebral body wedging, and disc wedging between the groups. Vertebral body shape was evaluated by computed tomography. Magnetic resonance and histology evaluated disc health. Biomechanical testing was performed to determine the effect of tensioning the tether on spinal motion and screw fixation. RESULTS: intraoperative tensioning produced immediate coronal deformity (8° ± 4° vs. 2° ± 1° in untensioned spines; P = 0.01) and apical disc (T9-T10) wedging, vertex on tethered side, (5° ± 2° vs. 2° ± 1°; P = 0.01). After 12 months, the groups were similar in coronal deformity (28° ± 18° pretensioned, 27° ± 11° untensioned, P = 0.88), sagittal deformity (25° ± 3° vs. 22° ± 3°; P = 0.14), vertebral body wedging (10° ± 5° vs. 8° ± 3°; P = 0.45), and disc wedging (-4° ± 1° vs. -4° ± 3°; P = 0.88). There was no radiographic evidence of screw loosening. One of the discs from each group had diminished T2 signal after 12 months of tethering. Tether pretensioning did not affect spinal stiffness or motion. Interestingly, screw fixation increased with pretensioning; however, there was no significant advantage with hydroxyapatite coating. Histology demonstrated normal-appearing discs. CONCLUSION: pretensioning of the tether created immediate deformity without effecting ultimate vertebral or disc deformity creation. Spinal motion and stiffness were not altered by pretensioning; however, pretensioning increased the torque required for screw extraction.

The present study was designed to test the hypothesis that blockade of angiotensin II type-1 receptors reduces oxidative stress and inflammation in patients with essential hypertension. The study population comprised 132 hypertensive patients, some receiving and others not receiving medical treatment. At enrollment their systolic and/or diastolic blood pressures were > or = 140 and/or > or = 90 mmHg, respectively. The serum concentration of C-reactive protein, and the urine concentrations of 8-epi-prostaglandin F2alpha and 8-hydroxydeoxyguanosine were measured at baseline and after 12 weeks of treatment either with an angiotensin II type-1 receptor blocker, candesartan (8 mg daily) (age 64 +/- 12 years; male/female 28/39; n = 67), or other antihypertensive agents that do not block the renin-angiotensin system (age 65 +/- 10 years, male/female 25/40, n = 65). Candesartan reduced the levels of C-reactive protein (from 0.07 +/- 0.04 [median value +/- median absolute deviation] to 0.06 +/- 0.03 mg/dl, p < 0.0001), 8-epi-prostaglandin F2alpha (from 210 +/- 92 to 148 +/- 59 pg/mg creatinine, p < 0.0001), and 8-hydroxydeoxyguanosine (from 5.7 +/- 1.9 to 4.0 +/- 1.3 ng/mg creatinine, p < 0.0001), while the levels of these markers were not altered after the treatment with other antihypertensive agents. Blood pressure decreased by a similar amount in both groups, and the reductions in the levels of the markers did not correlate with that of blood pressure. These results suggest that candesartan reduces oxidative stress and inflammation in hypertensive patients independently of its effects on blood pressure. This may provide useful information for determining therapeutic strategies to minimize tissue injury by inflammation and oxidative stress in hypertensive patients.

STUDY DESIGN: A rabbit model designed to investigate the effects of applied cyclic tensile stress on the cell division rate and the collagen synthesis in the rabbit nucleus pulposus cells in vitro. OBJECTIVE: To evaluate the effects of mechanical stress on nucleus pulposus cells, thus adding to the understanding of the adaptation of the intervertebral disc to mechanical stress. SUMMARY OF BACKGROUND DATA: Intervertebral disc cells in vivo are exposed to a multitude of physical forces during physical motion. Although it is known that in intervertebral disc disease, a common pathway of disc degeneration is mechanical stress on the nucleus pulposus or the anulus fibrosus or both, the underlying mechanism has been less well defined. METHODS: Nucleus pulposus cells were isolated from 4-week-old Japanese white rabbits. These cells were subjected to the mechanical cyclic stretch stress using a computerized, pressure-operated instrument that physically deformed the cells. The DNA synthesis rate, collagen synthesis rate, and cell cycle progression were measured. RESULTS: Cyclic tensile stretch increased the DNA synthesis rate in nucleus pulposus cells and in the population of cells in the S phase of the cell cycle during 1 to 2 days of subjugation to stress. Cyclic tensile stretch also increased collagenous protein synthesis in nucleus pulposus cells during 1 to 4 days of stress. CONCLUSIONS: Mechanical stress on nucleus pulposus cells promotes the proliferation of cells and alters the properties of intervertebral disc cells. This study may reflect the adaptation of the intervertebral disc to increased motion and stress.

The distribution of the extracellular matrix, including type I, III, IV and VI collagens and laminin, and of prolyl hydroxylase was investigated in the human endometrium by an indirect immunofluorescence method with specific monoclonal antibodies. Collagens were also extracted from the endometrial tissues in the proliferative and secretory phases and from the decidual tissues in the first trimester of pregnancy. Immunohistochemical studies demonstrated that interstitial collagens, such as type I, III, and VI collagens, were localized diffusely in the stroma of the endometrium throughout the menstrual cycle, as well as in the decidua. Type IV collagen and laminin were localized exclusively in the basement membrane of the endometrial glands and in the walls of blood vessels during the proliferative and secretory phases. However, strong staining for type IV collagen and laminin was recognized in the pericellular region of endometrial stromal cells in the decidua. Prolyl hydroxylase was localized in the cytoplasm of endometrial stromal cells and endometrial glandular cells during the menstrual cycle. Intense immunostaining for prolyl hydroxylase was observed in the decidual cells. However, immunoreactivity for prolyl hydroxylase in the endometrial glandular cells disappeared during the process of decidualization. The ratio of type III to type I collagen was significantly decreased (P < 0.05) and the ratio of type V to type I collagen was significantly increased (P < 0.01) in the decidua, as compared with ratios in the endometrium during the proliferative phase. The present results suggest that changes in the extracellular matrix may play an important role in implantation, in invasion of trophoblastic cells and in the maintenance of pregnancy.

BACKGROUND: BRCA1 is a tumor suppressor gene that is responsible for hereditary breast and ovarian carcinoma syndrome. The primary objective of the current study was to investigate the influence of BRCA1 expression on the prognoses of sporadic breast carcinomas. METHODS: A cohort of 175 Japanese women with invasive breast carcinoma who had no family history in first-degree relatives was studied. Expression of BRCA1 was determined by an immunohistochemical procedure in which the MS110 monoclonal antibody was used. Kaplan--Meier and Cox proportional regression survival analyses were used to compare negative and positive BRCA1 patients. RESULTS: One hundred fifteen (65.7%) of the 175 specimens showed positive BRCA1 staining (> 10% cells were immunoreactive). During a median follow-up of 4.4 years, negative BRCA1 patients had worse disease free survival than positive BRCA1 patients (35 % vs. 7%, respectively; P < 0.0001). BRCA1 expression was significantly inversely correlated with histologic grade (P < 0.0001) but not with lymph node status or other conventional prognostic markers. In multivariate analysis using the Cox regression model, positive BRCA1 emerged as an independent prognostic indicator for disease free survival. CONCLUSIONS: The results of this study suggest that BRCA1 may be a valuable marker for identifying women with sporadic breast carcinoma at high risk of developing recurrence, and who may be candidates for trials investigating new therapies in combination with standard adjuvant therapy.

Psychiatric nursing is a stressful area of nursing practice. The purpose of this study was to examine occupational stress among psychiatric nurses in Japan. In this cross-sectional study, 238 psychiatric nurses were recruited from 7 hospitals. Data regarding the Generic Job Stress Questionnaire (GJSQ), the Center for Epidemiologic Studies for Depression Scale (CES-D), and the Health Practice Index (HPI) were obtained via self-report questionnaires. After adjusting for all the variables, CES-D scores were associated with job stress, but social support reduced the effect of stress on depression among psychiatric nurses. However, the interpretation of these results was hampered by the lack of data concerning important occupational factors, such as working position, personal income, and working hours. Further longitudinal investigation into the factors associated with depression may yield useful information for administrative and psychological interventions.

STUDY DESIGN: To elucidate the pathomechanisms of radicular pain secondary to lumbar disc herniation. OBJECTIVES: To evaluate whether intervertebral disc material applied to the sciatic nerve produces hyperalgesia, and if the hyperalgesia in influenced by inhibitors of phospholipase A2 and nitric oxide synthase. SUMMARY OF BACKGROUND DATA: Previously, the authors reported that application of nucleus pulposus and anulus fibrosus material to the lumbar epidural space produces different forms of hyperalgesia (mechanical versus thermal), with different and distinct histologic changes. Additional pharmacologic studies showed that phospholipase A2 and nitric oxide are involved in the mechanisms that produce the mechanical and thermal hyperalgesia, respectively, N omega-nitro-L-arginine methyl ester and mepacrine are relatively selective inhibitors of nitric oxide synthase and phospholipase A2, respectively. However, it is not known what the relation is between the hyperalgesia produced and the activation and involvement of phospholipase A2 and production of nitric oxide, or why the application of nucleus pulposus and nucleus pulposus with anulus fibrosus produces different types of hyperalgesia. METHODS: Experiments were performed in five groups of rats: The control group (no treatment), the sham group (exposure of the sciatic nerve only), the fat group (allografted fat on the sciatic nerve), the nucleus pulposus group (allografted nucleus pulposus) and the nucleus pulposus + anulus fibrosus group (allografted nucleus pulposus and anulus fibrosus). Withdrawal threshold and latency from mechanical pressure and a radiant heat to hind paws were measured preoperatively and postoperatively. After local sciatic nerve administration of N theta-nitro-L-arginine methyl ester or mepacrine into the operated site, sensitivities to noxious stimuli were reevaluated after treatment. RESULTS: Only rats in the nucleus pulposus group showed evidence of mechanical hyperalgesia. However, injection of N theta-nitro-L-arginine methyl ester resulted in evidence of mechanical hyperalgesia in the nucleus pulposus + anulus fibrosus group. Mechanical hyperalgesia was produced in the nucleus pulposus group and after injection of N theta-nitro-L-arginine methyl ester in the nucleus pulposus+anulus fibrosus group, both of which returned to normal after mepacrine injection. There were no significant changes in sensitivity to thermal stimuli in any of the experimental groups. CONCLUSION: It appears that phospholipase A2 and nitric oxide play important but different roles in pathomechanisms of radicular pain in lumbar disc herniation.

BACKGROUND AND OBJECTIVE: While recent studies have shown that patients with COPD and patients with asthma exhibit evidence of airway and systemic inflammation, markers of systemic inflammation have not been compared between the two diseases. METHODS: To evaluate circulating inflammatory markers, blood was sampled from 111 patients with COPD, 75 control subjects and 46 asthmatic patients (some of whom were smokers). Measurements of WCC, serum levels of fibrinogen, high-sensitivity (hs)-CRP, IL-8, IL-6, tumour necrosis factor-alpha (TNF-alpha), transforming growth factor (TGF)-beta1, tissue inhibitors of metalloproteinase (TIMP)-1, neutrophil elastase and alpha1-antitrypsin (alpha1-AT) were performed. RESULTS: Serum TNF-alpha, IL-6 and TIMP-1 concentrations were significantly higher in patients with stable COPD and patients with asthma than in control patients. Serum alpha1-AT levels were significantly higher in COPD patients than in asthmatic patients and control subjects, and serum TGF-beta1 levels were higher in asthma patients than in COPD patients. Smoking status had no effect on markers in COPD and asthmatic patients. CONCLUSIONS: Although COPD and asthma share common markers of systemic inflammation, serum levels of TGF-beta1 and alpha1-AT may reflect differences between the diseases.