Lumbar spinal root compression caused by Brucella granuloma

Myospherulosis is a rare condition. The authors report a unique case of this entity arising in paranasal sinus. The review of literature with emphasis on pathogenesis is also discussed.     

Glucosamine-induced insulin resistance in 3T3-L1 adipocytes is caused by depletion of intracellular ATP

Glucosamine, which enters the hexosamine pathway downstream of the rate-limiting step, has been routinely used to mimic the insulin resistance caused by high glucose and insulin. We investigated the effect of glucosamine on insulin-stimulated glucose transport in 3T3-L1 adipocytes. The Delta-insulin (insulin-stimulated minus basal) value for 2-deoxyglucose uptake was dramatically inhibited with increasing concentrations of glucosamine with an ED50 of 1.95 mM. Subcellular fractionation experiments demonstrated that reduction in insulin-stimulated 2-deoxyglucose uptake by glucosamine was due to an inhibition of translocation of both Glut 1 and Glut 4 from the low density microsomes (LDM) to the plasma membrane. Analysis of the insulin signaling cascade revealed that glucosamine impaired insulin receptor autophosphorylation, insulin receptor substrate (IRS-1) phosphorylation, IRS-1-associated PI 3-kinase activity in the LDM, and AKT-1 activation by insulin. Measurement of intracellular ATP demonstrated that the effects of glucosamine were highly correlated with its ability to reduce ATP levels. Reduction of intracellular ATP using azide inhibited Glut 1 and Glut 4 translocation from the LDM to the plasma membrane, insulin receptor autophosphorylation, and IRS-1 tyrosine phosphorylation. Additionally, both the reduction in intracellular ATP and the effects on insulin action caused by glucosamine could be prevented by the addition of inosine, which served as an alternative energy source in the medium. We conclude that direct administration of glucosamine can rapidly lower cellular ATP levels and affect insulin action in fat cells by mechanisms independent of increased intracellular UDP-N-acetylhexosamines and that increased metabolism of glucose via the hexosamine pathway may not represent the mechanism of glucose toxicity in fat cells.     

Thoracic outlet compression syndrome caused by a schwannoma of the C7 nerve root

This is the first report of a schwannoma originating from the C7 nerve root causing thoracic outlet compression syndrome. The patient was a 30-year-old woman with a 3-year history of numbness on the radial side of the left hand, left arm tiredness, nocturnal pain in the left forearm and pain in the left elbow, shoulder and neck. Conservative treatment and previous operations, including carpal tunnel release and first rib resection, provided no relief. A left scalenectomy was performed. During the removal of the anterior scalene muscle, a mass approximately 3 cm long and 1.5 cm in diameter was noted under the anterior scalene muscle involving the C7 nerve root. The tumour was encapsulated and covered with attenuated and stretched nerve fascicles. It was completely excised without disturbing the nerve fascicles. The clinical impression was schwannoma, which was confirmed on pathological examination.     

Endothelin-stimulated Ca2+ mobilization by 3T3-L1 adipocytes is suppressed by tumor necrosis factor-alpha

The cytokine tumor necrosis factor-alpha (TNFalpha) contributes to metabolic changes in disease states such as insulin resistance. However, the mechanism by which TNFalpha alters cellular function in these conditions is poorly understood. Because changes in intracellular calcium concentration plays a critical role in hormone action we investigated the effect of TNFalpha on calcium homeostasis in 3T3-L1 adipocytes. In these studies we show that TNFalpha causes a concentration- and time-dependent decrease in Na+/myo-inositol cotransporter (SMIT) mRNA levels and myo-inositol accumulation as well as a decrease in myo-inositol incorporation into phosphoinositides. These changes coincided with a decrease in endothelin-1-induced phosphatidylinositol (PI) cycle activity in 3T3-L1 adipocytes chronically exposed to TNFalpha. Endothelin-1-induced mobilization of calcium from intracellular stores was also diminished by TNFalpha. The effect of TNFalpha on endothelin-1-induced PI cycle activity and calcium mobilization was not due to a decrease in endothelin receptors. However, TNFalpha did cause a moderate decrease in phosphatidylinositol 4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) activity in 3T3-L1 adipocytes. Combined, a decrease in phosphoinositide production and PIP2-specific PLC activity could be responsible for altering PI cycle activity and the generation of the second messenger myo-inositol 1,4,5-trisphosphate, thereby reducing calcium mobilization. Such changes in intracellular signaling may contribute to the pathophysiology of insulin resistance associated with TNFalpha.     

Lumbar spinal canal stenosis associated with progressive degenerative changes of the spine. A case report

STUDY DESIGN: Case report. OBJECTIVES: To report a case of spinal canal stenosis associated with progressive degenerative changes of the lumbar spine. SUMMARY OF BACKGROUND DATA: As far as the authors are aware, there has been no similar case reported. METHODS: The clinical features of the case are reported, and the pathology is discussed. RESULTS: In a 40-year-old man, spinal canal stenosis developed, associated with progressive degenerative changes of the lumbar spine. The man underwent posterior decompression and fusion using pedicle screws. The surgical results were satisfactory at the time of writing this report. CONCLUSIONS: This case presented a peculiar clinical course, which could not be categorized under previously reported disorders. It may be a new disease entity of spinal canal stenosis. The surgical outcome was satisfactory 2 years, 6 months after surgery.     

Cervical spinal cord compression caused by ossification of the posterior vertebral ligament. Apropos of a case

In eight Japanese patients, three different laparoscopic procedures were used to excise an early gastric carcinoma; partial resection in four, intragastric resection of the gastric mucosa in two, and laparoscopic-assisted distal partial gastrectomy with the abdominal wall-elevating method in two patients. Histological examinations revealed that the lesions were completely resected, and there was no evidence of lymphatic metastasis. The operation time ranged from 2 to 4 h. These forms of laparoscopic gastric surgery for patients with early gastric carcinomas may be useful from the standpoint of minimal access, rapid recovery, less pain, and good cosmesis.     

Cytosolic and nuclear distribution of PPARgamma2 in differentiating 3T3-L1 preadipocytes

In light of the pivotal role that PPARgamma2 plays in the expression of fat specific genes (e.g., A-FABP), we have examined the hypothesis that a rise in PPARgamma2 protein is required for the expression of A-FABP, and that the acceleration of fat cell differentiation by the thiazolidinedione agent, pioglitazone (PIOG), reflects an increase in the abundance of PPARgamma2 mRNA and protein. Western analyses surprisingly revealed that undifferentiated 3T3-L1 fibroblasts contained significant levels of PPARgamma2 protein; that the amount of total cellular PPARgamma2 only increased 2-fold during differentiation; and that the levels of PPARgamma2 protein and mRNA were not increased by PIOG even though fat cell differentiation was accelerated by PIOG as revealed by a 20-fold increase in A-FABP expression. Cell fractionation studies revealed that PPARgamma2 was evenly distributed between the cytosolic and nuclear compartments in both undifferentiated and differentiating 3T3-L1 cells. Immunocytochemical studies with a PPARgamma2-specific antibody indicated that PPARgamma2 was diffusely distributed throughout the cytosol of undifferentiated 3T3-L1 cells, but as the differentiation progressed, the PPARgamma2 became focused around the developing lipid droplets. In contrast to PPARgamma2, undifferentiated 3T3-L1 cells contained no measurable quantities of RXRalpha, but once fat cell differentiation was initiated by treatment with IBMX and dexamethasone, the cellular content of RXRalpha increased several fold. The rise in RXRalpha content paralleled the induction of A-FABP, but the expression of RXRalpha was not enhanced by PIOG. Although the amount of PPARgamma2 and RXRalpha was unaffected by PIOG, gel shift assays revealed that PIOG stimulated PPARgamma2/RXRalpha binding to the adipose response element of A-FABP by 5-fold in less than 12 h. Apparently, RXRalpha rather than PPARgamma2 is the pivotal trans-factor essential for the initiation of terminal fat cell differentiation. However, the high cytsolic content of PPARgamma2 and its association with the lipid droplet of differentiating 3T3-L1 cells suggests PPARgamma2 may possess a cytosolic function in the developing fat cell.     

Ginsenosides increase secretion of lipoprotein lipase by 3T3-L1 adipocytes

Treatment of 3T3-L1 adipocytes with either an oleanolic acid glycoside or a 20(S)-protopanaxatriol glycoside increased the secretion of lipoprotein lipase activity into the medium dose-dependently. At a concentration of 100 micrograms/ml, ginsenosides Ro, Re, Rg1, and Rh1 increased the secretion of lipase activity into the medium by 119, 107, 56, and 32%, respectively. The ratio of lipase activity in the medium to cellular lipase activity was 4.7% in control cells and 8.6% in ginsenoside Ro-treated cells, 8.3% in ginsenoside Re-treated cells, 7.0% in ginsenoside Rg1-treated cells, and 6.3% in ginsenoside Rh1-treated cells. Ginsenoside Rb2, which is a 20(S)-protopanaxadiol glycoside, increased the secretion of lipase activity by 16% at 25 micrograms/ml, and the ratio of lipase activity in the medium to cellular lipase activity was higher in ginsenoside Rb2-treated cells than in control cells. However, at 100 and 200 micrograms/ml, ginsenoside Rb2 decreased the secretion of lipase activity in parallel with cellular lipase activity. Ginsenoside Rd also decreased the secretion of lipase activity in the same dose-dependent manner. Thus, the effective dose for the secretion of lipoprotein lipase activity with ginsenosides varies with their aglycone structure.     

马钢冷轧硅钢生产线自动化控制及L2-L3接口的实现

主要介绍了马钢股份有限公司第一钢轧总厂冷轧硅钢生产线一级,二级控制系统构成,实现的主要功能,三级生产制造执行系统的功能扩充,以及L2-L3接口通信程序的实现。     

Gateway在梅钢热轧L2-L3通讯接口中的应用

阐述了基于通讯平台的gateway中间件产品的通讯方式和故障诊断功能，并着重介绍了该中间件在梅钢热轧L2-L3接口设计中的应用。该中间件的故障诊断方法为热轧L2-L3通讯接口提供了切实有效的调试平台。     

Clinical analysis of two-level compression of the cauda equina and the nerve roots in lumbar spinal canal stenosis

STUDY DESIGN: This study is a prospective, clinical study assessing the efficacy of selective decompression of the responsible level in two-level stenosis in accordance with neurologic findings defined by the gait load test, and functional diagnosis based on selective nerve root block. OBJECTIVE: To clarify the clinical features of two-level stenosis regarding the neurologic level responsible for the symptoms, neurogenic intermittent claudication, and the outcome of selective decompression. SUMMARY OF BACKGROUND DATA: Experimental studies have indicated that double-level compression of the cauda equina induces a more severe impairment of nerve function than does single-level compression. However, few studies have focused on the clinical importance of two-level stenosis. The clinical effects of two-level stenosis on the cauda equina and nerve roots are unknown. METHODS: A total of 81 patients with lumbar spinal canal stenosis due to spondylosis and degenerative spondylolisthesis were divided into two groups, two-level stenosis at L3-L4 and L4-L5, and one-level stenosis at L4-L5, based on myelography. The types of neurogenic intermittent claudication, the level responsible for neurologic findings, and the postsurgical outcome were compared between both groups. The level responsible for the symptoms in two-level stenosis was determined in accordance with neurologic findings on the gait load test and functional diagnosis based on a selective nerve root block. All patients underwent a prospective, selective decompression at the neurologically responsible level only. The average follow-up period was 4.6 years (range, 1-8 years). RESULTS: The patients with two-level stenosis more frequently had cauda equina symptoms than those with one-level stenosis, except patients with degenerative spondylolisthesis. It was therefore assumed that two-level stenosis was associated with cauda equina impairment, Changes in neurologic condition before and after the gait test were observed in four patients with two-level stenosis. Finally, for 28 patients with two-level stenosis, the levels responsible for the neurologic symptoms were the caudal level (L4-L5) in 22 patients, the cranial level (L3-L4) in 1 patient, and both cranial and caudal levels (L3-L4 and L4-L5) in 5 patients. All stenotic levels on the myelogram were not always symptomatic in two-level stenosis. However, in one-level stenosis, all of the responsible levels completely corresponded to the myelogram. Selective decompression only at the neurologically responsible level improved neurogenic intermittent claudication in all patients. The asymptomatic levels at which the stenotic condition was left unchanged at surgery did not become symptomatic at follow-up; in addition, there was no significant difference in the postoperative outcome between two-level stenosis and one-level stenosis. CONCLUSIONS: Two-level stenosis in patients with lumbar spondylosis is associated with production of cauda equina lesions. The gait load test provides information regarding changes in symptoms and neurologic condition during exercise. The responsible levels should be determined based on neurologic findings after the gait load test and a selective nerve root block. It is uncommon for both stenotic levels to be symptomatic in patients with two-level stenosis. Less invasive surgery such as selective decompression for the responsible level in patients with two-level stenosis is a useful technique with a good potential for long-term success.     

Dehydroepiandrosterone reduces proliferation and differentiation of 3T3-L1 preadipocytes

In this study we analyzed photosensitizing and photodamaging properties of the hydrophobic meso-tetraphenylporphyrin (TPP, incorporated into liposomes) on HeLa cells. Under the fluorescence microscope, red fluorescence by TPP was detected on the cell surface. TPP followed by violet-blue or red irradiation led to cell death, blebs and plasma membrane deformations appearing immediately after photodynamic treatment. Production of singlet oxygen by TPP was studied by analyzing tryptophan photodegradation, which increased in the presence of D2O and was abolished by NaN3. Present results suggest that the plasma membrane is the main cellular target for TPP, which could be a valuable photosensitizing drug in studies on photodynamic therapy of cancer.     

马钢2#连续热镀锌生产线自动化控制及L1-L4联动关键技术的实现

主要介绍了马钢第一钢轧总厂冷轧薄板2#连续热镀锌生产线一级和二级控制系统的构成、实现的基本功能、三级控制系统的功能扩充以及L1—L4关键技术-L2-L3接口的开发,实现生产全程控制和企业综合信息化。     

Nutrient control of GLUT1 processing and turnover in 3T3-L1 adipocytes

Metabolic labeling and immunoprecipitation were used to analyze the glucose-dependent regulation of GLUT1 synthesis, processing, and turnover in a murine adipocyte cell line. Metabolically labeled GLUT1 from control cells migrated as a 46-kDa protein, while GLUT1 from cells deprived of glucose for more than 12 h migrated as a 37-kDa protein. On the basis of tunicamycin sensitivity, both GLUT1 species arose from a common protein migrating at 36 kDa. In addition, the rate of synthesis of GLUT1 in control and glucose-deprived cells was similar. In short pulse-chase experiments, we distinguished two species arising from the core GLUT1 protein in control cells; an intermediate and the mature 46-kDa species. In contrast, only one glycoform, the 37-kDa species, arose from the core protein in glucose-deprived cells, which was not further processed in either the presence or absence of glucose. Although 12-18 h of glucose deprivation were required to affect GLUT1 glycosylation, glucose-deprived cells quickly recovered the ability to correctly glycosylate GLUT1 upon the readdition of glucose (t1/2 < 1 h). GLUT1 in control adipocytes exhibited a half-life of approximately 14 h, while that in glucose-deprived adipocytes was greater than 50 h. This effect was readily reversed upon the readdition of glucose. In total, these data show that glucose deprivation alters both the processing (glycosylation) and turnover (degradation) of GLUT1. These results are discussed in light of transport function.     

Duodenal trichobezoar caused by compression of the superior mesenteric artery

Trichobezoars can occur in young women who have a history of trichotillomania, trichophagia, gastric dysmotility, and psychiatric dysfunction. A 6-year-old anorexic girl presented with a fixed right-upper-quadrant abdominal mass. Exploratory celiotomy for a duodenal trichobezoar led to removal of the large foreign body, via a duodenotomy, and prompted a Ladd procedure, in which the duodenum was moved from beneath the compressing superior mesenteric artery to relieve underlying duodenal narrowing.