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Biomedical subjects

N Tong

Publications and source records attributed to N Tong.

At least 19 recordsLinked to original sources
PubMed2005

Muscle infarction involving muscles of abdominal and thoracic walls in diabetes.

AIMS: This paper presents two cases of muscle infarction involving four major muscles of the anterior abdominal wall (case 1) and pectoralis major (case 2) in individuals with diabetes. METHODS: Erythrocyte sedimentation rate (ESR) and creatine kinase (CK) were measured and Doppler ultrasound, an open muscle biopsy (case 1) and magnetic resonance imaging (MRI) (case 2) were performed. RESULT: The diagnosis of muscle infarction was made by histological findings and MRI images with hyper-intensive signals on a gadolinium-enhanced T2-weighted sequence, respectively. Both patients were treated with bed rest, immobilization of the involved extremities, analgesia and intensive insulin therapy. In addition, anticoagulant drugs such as low molecular weight heparin sodium and cilostazol, and some traditional Chinese medicines such as ligustrazine and salvia miltiorrhiza were administered. The symptoms of both patients resolved gradually after 3 weeks. However, muscle infarction reoccurred in case 1 on the opposite side of the abdomen and recovered after 40 days. CONCLUSIONS: This is the first report of muscle infarction involving the muscles of anterior abdominal walls and pectoralis major in diabetes. MRI is the best non-invasive technique and T2-weighted imaging is the most valuable method for the diagnosis. In addition to supportive therapy, administration of anticoagulant agents and some Chinese traditional medicine may be useful in symptom relief.

Abdominal Muscles↗
PubMed2001

Activation of glycogen synthase kinase 3 beta (GSK-3beta) by platelet activating factor mediates migration and cell death in cerebellar granule neurons.

Children with vertically acquired HIV-1 can present with a rapidly progressive encephalopathy and neuronal apoptosis in the first 12-18 months of life. Furthermore, abnormal prenatal platelet activating factor (PAF) signalling may result in lissencephaly, a disorder of neuronal migration. PAF, produced from human immunodeficiency virus type 1 (HIV-1) -infected brain-resident macrophages, induces neuronal apoptosis in cultured cerebellar granule neurons (CGNs) in part by activating glycogen synthase kinase 3 beta (GSK-3beta). However, PAF can also inhibit migration of CGNs that are dispersed and allowed to reaggregate. Therefore, we investigated the biological effects following activation of GSK-3beta by PAF, and whether these effects were dependent on the culture conditions of the CGNs. We show here that activation of neuronal GSK-3beta by PAF is receptor-specific, with similar kinetics of activation in both monolayer cultures of CGNs that have ceased to migrate and reaggregate cultures of CGNs that are actively migrating. However, PAF receptor activation in reaggregated CGNs inhibits neuronal migration and induces approximately half the level of neuronal apoptosis compared with PAF-treated CGN cultures that have ceased to migrate. PAF-mediated inhibition of neuronal migration in reaggregated CGNs or induction of apoptosis in CGNs that have ceased to migrate can be reversed by either PAF receptor antagonists, or the GSK-3beta inhibitors lithium or valproic acid, in a dose-dependent manner. Abnormal PAF signalling that results in GSK-3beta overactivation may represent a common mechanism for pathological defects in neuronal migration in the prenatal period and neuronal apoptosis in the postnatal period.

Animals↗
PubMed2001

[Gigantism with low serum level of growth hormone: a case report].

Gigantism with low or normal basal concentrations of growth hormone (GH) is a rare condition, possibly due to abnormal GH secretory patterns, enhanced tissue sensitivity to GH, or the existence of an unidentified growth promoting factor. Here we report an 11 year-old female case of gigantism with a normal pituitary gland. Her height was 181 cm, body weight 77 kg, and bone age 11.1 years. Her basal serum GH levels were lower than 1 ng/ml. The levels of T3, T4, FT3, FT4, TSH, E2, LH, FSH, PRL, PTC and ACTH were normal. Serum GH response to insulin-induced hypoglycemia or arginine stimulation tests was blunted. In this case, non-pulsatile GH secretion and enhanced tissue sensitivity to GH may induce hypersecretion of IGF-1 and the existence of an unidentified growth promoting factor or biologically active anti-GH receptor antibodies may cause clinical gigantism.

Child↗
PubMed2001

[Study on gastric motility and its relevant factors in type 2 diabetes].

OBJECTIVE: In this study radionuclide semi-liquid gastric emptying (GE) study was adopted to test the gastric motility in 129 patients with type 2 diabetes. Further study was made to explore the relationship between gastric motility disorder of diabetes and the influential factors. METHODS: The variables to be measured and analyzed were age, BMI, duration of illness, level of glycemia, HbAlc, plasma insulin, motilin, gastrin, glucagon and Mg2+. RESULTS: Of the 129 cases, 80 had delayed GE with an occurrence of 62.02%, and there was a close correlation between gastric motility disorder and the duration of illness, BMI, FPG, PPG, serum insulin, motilin levels and HbAlc as well. CONCLUSION: These findings imply that gastric motility disorder of diabetes is influenced by multiple factors. The results also suggest that gastric motiligy disorder is much more common than expected, and radionuclide gastric emptying test is a useful aid for the early detection of this clinical entity.

Adult↗
PubMed2001

[A multicenter randomized controlled clinical trial on lipids regulating effects of domestic simvastatin].

OBJECTIVE: This clinical trial was designed to assess the lipids regulating effects of domestic simvastatin (DS, produced by Chengdu Huayu Pharmaceutical Co.) in patients with hyperlipidemia. METHODS: 160 hyperlipidemic patients were randomly divided into 3 groups (A, B and C). Groups A and B were subjected to single-blind trial; group C was for open trial. Group A took DS 10 mg q.n., group B Zocor 10 mg q.n. and group C DS 10 mg q.n. respectively for 8 weeks. All the patients were followed up at the 4th week and 8th week. 155 patients finished the trial with 59 cases in group A, 47 cases in group B and 39 cases in group C. RESULTS: At the 4th week, serum total cholesterol (TC) in group A, B and C decreased by 16.88%, 19.23% and 14.10%; serum triglycerides (TG) decreased by 19.27%, 15.66% and 17.96%; HDL-C increased by 7.69%, 7.46% and 6.69%; and LDL-C decreased by 23.02%, 27.84% and 24.43%, respectively; there was no significant difference among the three groups (P > 0.05). At the 8th week, serum TC in groups A, B and C decreased by 25.03%, 26.53% and 25.22%. TG decreased by 23.85%, 24.74% and 24.75%; HDL-C increased by 9.23%, 8.95% and 8.39%; and LDL-C decreased by 33.72%, 35.50% and 30.99%, respectively; still, no significant difference among the three groups was observed (P > 0.05). The incidence rates of side effects in the three groups were similar. The clinical effects were more significant at the 8th week than at the 4th week for Zocor and DS. CONCLUSION: These data suggest that DS is as effective and safe as Zocor in clinical use for lipids regulating serum.

Adult↗
PubMed2000

Hospital pharmacy service provision in Australia--1998.

The results of a 1998 national survey of pharmaceutical services in hospitals throughout Australia are reported. A self-administered questionnaire was sent to all directors of hospital pharmacy services and senior hospital pharmacy managers to determine the extent of clinical and nonclinical pharmacy services provided by hospitals in Australia. Respondents chose the services their departments provide from a list of 26 commonly provided services. The response rate was 58.5%. Respondents were fairly evenly divided between teaching and nonteaching hospitals, but most of the respondents were from public (versus nongovernment) hospitals. The five most commonly provided services were imprest (a wordstock of frequently used medications that are regularly restocked by the pharmacy department), informal drug education for hospital staff, review of medication charts, control of drug purchasing, and inpatient dispensing. Review of medication charts and provision of drug education for the hospital staff were the most widely provided clinical pharmacy services. The most common services available from hospital pharmacies throughout Australia were imprest, informal drug education for hospital staff, review of medication charts, control of drug purchasing for the hospital, and inpatient dispensing.

Australia↗
PubMed2000

Neuronal fractalkine expression in HIV-1 encephalitis: roles for macrophage recruitment and neuroprotection in the central nervous system.

HIV-1 infection of the brain results in chronic inflammation, contributing to the neuropathogenesis of HIV-1 associated neurologic disease. HIV-1-infected mononuclear phagocytes (MP) present in inflammatory infiltrates produce neurotoxins that mediate inflammation, dysfunction, and neuronal apoptosis. Neurologic disease is correlated with the relative number of MP in and around inflammatory infiltrates and not viral burden. It is unclear whether these cells also play a neuroprotective role. We show that the chemokine, fractalkine (FKN), is markedly up-regulated in neurons and neuropil in brain tissue from pediatric patients with HIV-1 encephalitis (HIVE) compared with those without HIVE, or that were HIV-1 seronegative. FKN receptors are expressed on both neurons and microglia in patients with HIVE. These receptors are localized to cytoplasmic structures which are characterized by a vesicular appearance in neurons which may be in cell-to-cell contact with MPs. FKN colocalizes with glutamate in these neurons. Similar findings are observed in brain tissue from an adult patient with HIVE. FKN is able to potently induce the migration of primary human monocytes across an endothelial cell/primary human fetal astrocyte trans-well bilayer, and is neuroprotective to cultured neurons when coadministered with either the HIV-1 neurotoxin platelet activating factor (PAF) or the regulatory HIV-1 gene product Tat. Thus focal inflammation in brain tissue with HIVE may up-regulate neuronal FKN levels, which in turn may be a neuroimmune modulator recruiting peripheral macrophages into the brain, and in a paracrine fashion protecting glutamatergic neurons.

Adult↗
PubMed2000

Functional interplay between nuclear factor-kappaB and c-Jun integrated by coactivator p300 determines the survival of nerve growth factor-dependent PC12 cells.

Nerve growth factor (NGF) activates the transcription factors nuclear factor kappaB (NF-kappaB) and activator protein-1 (AP-1) in sympathetic neurons. Whereas NGF-inducible NF-kappaB is required for the survival of neurons, c-Jun has the ability to promote neuronal death. In this report, we have examined the effect of NGF withdrawal on c-Jun and NF-kappaB transcription factors in PC12 cells differentiated to a neuronal phenotype. We show that the withdrawal of NGF from these cultures results in de novo synthesis of c-Jun, increase in AP-1 activity, and down-regulation of NF-kappaB activity. To investigate how the signal transduction pathways activating c-Jun and NF-kappaB are differentially regulated by NGF, we performed transcriptional analyses. Expression of ReIA (NF-kappaB) suppressed the c-Jun-dependent transcription of c-jun, and this effect was reversed by overexpression of the coactivator p300. RelA's effects on c-Jun transcription were mediated by competitive binding of the carboxy-terminal region of RelA to the CH1 domain of p300, which also binds to c-Jun; deletion of this region abrogated the ability of RelA to inhibit c-Jun activity. Furthermore, the inhibition of endogenous NF-kappaB in NGF-maintained neuronal PC12 cells led to the induction of c-Jun synthesis and a marked increase in cell death. Together, these studies demonstrate a functional interaction between NF-kappaB and c-Jun and suggest a novel mechanism of NF-kappaB-mediated neuroprotection.

Animals↗
PubMed2000

Release of the neuronal glycoprotein ICAM-5 in serum after hypoxic-ischemic injury.

Intercellular adhesion molecule (ICAM)-5 (telencephalin) is unique among the ICAMs, because it is only expressed in somatodendritic membranes of telencephalic neurons. To investigate the fate of ICAM-5 during focal brain injury, we induced hypoxia-ischemia (HI) damage in adult mice by right common carotid artery ligation followed by hypoxia. ICAM-5 was detectable in serum within a 48-hour window after HI injury. In HI brain, dendritic ICAM-5 immunore-activity was abolished, but it was present in the neuropil and soma of hippocampal pyramidal, dentate granule, and some cortical and striatal neurons. After HI injury, levels of ICAM-5 protein and messenger RNA initially increased, and ICAM-5 messenger RNA expression then decreased, although protein levels continued to increase. Because HI injury induces microglial activation with increases in CD11a/CD18 (lymphocyte function antigen [LFA]-1) counterreceptors to ICAM-5, we investigated whether modulation of interactions between LFA-1 receptors and brain ICAM-5 during HI injury are associated with changes in levels of serum ICAM-5. Intracerebroventricular administration of lipopolysaccharide to activate microglia before HI injury resulted in elevated serum ICAM-5 levels compared with those in mice with only HI injury. Pretreatment with anti-LFA-1 antibodies before HI injury or LFA-1 receptor knockout mice with HI injury had markedly reduced levels of serum ICAM-5. Lipopolysaccharide levels increased, whereas LFA-1 receptor blockade or LFA-1 knockout decreased HI injury in the first 12 hours. These data suggest that during the necrotic phase of HI injury, serum ICAM-5 may be a potential marker for somatodendritic neuronal damage.

Animals↗
PubMed1999

HIV-1 Tat-mediated activation of glycogen synthase kinase-3beta contributes to Tat-mediated neurotoxicity.

Human immunodeficiency virus type 1 (HIV-1) Tat induces neuronal apoptosis. To examine the mechanism(s) that contribute to this process, we studied Tat's effects on glycogen synthase kinase-3beta (GSK-3beta), an enzyme that has been implicated in the regulation of apoptosis. Addition of Tat to rat cerebellar granule neurons resulted in an increase in GSK-3beta activity, which was not associated with a change in protein expression and could be abolished by the addition of an inhibitor of GSK-3beta (lithium). Lithium also enhanced neuronal survival following exposure to Tat. Coprecipitation experiments revealed that Tat can associate with GSK-3beta, but direct addition of Tat to purified GSK-3beta had no effect on enzyme activity, suggesting that Tat's effects might be mediated indirectly. As the activation of platelet activating factor (PAF) receptors is critical for the induction of neuronal death by several candidate HIV-1 neurotoxins, we determined whether PAF can also activate GSK-3beta. Application of PAF to neuronal cultures activated GSK-3beta, and coincubation with lithium ameliorated PAF-induced neuronal apoptosis. These findings are consistent with the existence of one or more pathways that can lead to GSK-3beta activation in neurons, and they suggest that the dysregulation of this enzyme could contribute to HIV-induced neuronal apoptosis.

Animals↗
PubMed1999

[A pair-matched comparison and follow-up study of patients with euthytroid Graves ophthalmopathy and patients with hyperthyroid graves ophthalmopathy].

This study was intended to acquire a knowledge about the similarity and difference between euthyriod Graves ophthalmopathy (EGO) and hyperthyroid Graves ophthalmopathy (HGO), and about the outcome of the EGO cases. Twenty-seven EGO patients were pair-matched with 27 HGO patients, and 18 of the EGO patients were followed up for 1-6 years. The results showed that the EGO group had markedly more patients with diplopia, failure to close lids, limitation of eyeball movements, cornea involvement, and more patients with a difference of two eyes' exophthalmos degrees > or = 2 mm, but the HGO group had more patients with optic nerve involvement. No significant difference was found between the two groups' ophthalmopathic indexes by using the t-test. Drug therapy of the EGO group was more efficacious than that of the HGO group. The results of follow-up study showed that 61% of the EGO cases had hyperthyroidism and goiter within 5 months to 3 years, but 39% of the cases had no hyperthyroidism up to 6 years. These data suggest that EGO is associated with thyroid diseases and it can stand "alone" as an auto-immune disease.

Adolescent↗
PubMed1999

[A clinical study of sudden death in patients with type 2 diabetes mellitus].

This study aimed to investigate the clinical characteristics of sudden death (SD) in type 2 diabetes mellitus (DM2). Clinical data from 1988 through 1996 in our hospital showed that 130 hospitalized patients with DM2 died, and 17 of them died of SD (13.08%). These 17 SD patients were pair-matched with 17 DM2 patients who were alive in the same period. The results revealed that the SD group had longer clinical DM duration, more chronic diabetic complications and higher blood pressure. In the direct causes of SD, cardiac SD accounted for 76.47%. The others were non-cardiac factors, including cerebral hemorrhage, hyperkalemia from diabetic nephropathy with renal failure and respiratory tract obstruction from lung infection. The triggering causes included eating, defecting, lung infection, strenuous attempt, hypoglycemia and surgical operation. To reduce the rate of SD in DM2, it is necessary and vital to treat the DM2 itself, and to take positive steps to prevent the onset of SD in high risk patients.

Aged↗
PubMed1998

M protein correlates with the receptor-binding specificity of haemagglutinin protein of reassortant influenza A (H1N1) virus.

From the reassortment experiments between A/Aichi/4/92 and A/WSN/33 (WSN) (H1N1) viruses, two different phenotype viruses which contained the haemagglutinin (HA) gene from A/Aichi/4/92 virus and the neuraminidase (NA) gene from WSN virus were obtained. PW13 and PW15 viruses agglutinated chicken red blood cells (CRBC), while PW10 and PW70 viruses did not. However, the expressed HA proteins of these viruses did not adsorb CRBC. The difference in gene constellation between PW13, PW15 and PW10, PW70 viruses was the membrane protein (M) gene. The former two had the M gene from A/Aichi/4/92 virus and the latter two had that from WSN virus. In PW15-infected cells, haemadsorption of CRBC was observed 30 min later than that of goose red blood cells and the M1 protein migrated from the nucleus to the cytoplasm 30 min earlier than adsorption of CRBC was observed. On the other hand, in PW10-infected cells, haemadsorption of CRBC was not observed through the virus replication and the M1 protein stayed in the nucleus after HA and NA activities reached maximum levels. Co-expression of the M and the HA proteins of A/Aichi/4/92 virus did not help the HA protein gain the ability to adsorb CRBC. However, neuraminidase treatment of COS cells expressing the HA protein of A/Aichi/4/92 virus or MDCK cells infected by PW10 virus restored the ability to adsorb CRBC. We discussed the possibility that the M1 protein helped the NA protein in its role to modify the HA protein on the cell surface.

Agglutination↗
PubMed1997

[Changes of serum TNF-alpha level, t-PA activivty and PAI activity in patients with silent myocardial ischemia or silent cerebral ischemia].

Tumor necrosis factor-alpha (TNF-alpha) level, tissue-typed plasminogen activator(t-PA) activity and PA inhibitor (PAI) activity were determined in three groups: (1) 25 NIDDM patients with silent myocardial ischemia (SMI) or silent cerebral ischemia (SCI); (2) 18NIDDM patients without SMI or SCI; (3) 20 age-matched normal controls. Diagnosis of SMI or SCI was based on the finding of ischemic evidence by SPECT of myocardiotomograph or cerebrotomograph. All patients ECG and blood pressure were normal, and they had no history of clinical symptoms and signs of MI or CI. The result showed that the TNF-alpha level and PAI activity in the ischemia group were the highest and the t-PA activity in the ischemia group was the lowest, as compared with those in the other two groups respectively. It suggests that in NIDDM patients who have high TNF-alpha, high PAI activity, low t-PA, and even no symptoms and signs of MI or CI, anticoagulant therapy might be useful to prevent the progression of diabetic macroangiopathies.

Brain Ischemia↗
PubMed1996

[The effects of intensive DMPA regimen in the treatment of Graves' ophthalmopathy].

35 patients with Graves' ophthalmopathy were treated with DMPA regimen which included dexamethasone (D) 20-30 mg and Methotrexate (M) 15-20 mg i.v. once a week and prednisone (P) 20 mg/d p. o. 4 times a week for 4 weeks followed by addition of azathioprine (A) or 6-MP 75-100 mg/d and the increment of prednisone (20 mg/d) to 5 times a week in the fifth and sixth weeks. The full intensive course of therapy lasted for 6 weeks. If necessary, the similar course of therapy might be repeated. Later on, each patient was mintainted on a therapy with P and A or P and 6-MP for another 1-2 months then the P and A or P and 6-MP for another 1-2 months, and then the P and A or 6-MP were tapered and finally discontinued at the end of sixth month. The symptoms and signs of the opthalmopathy were evaluated blindedly at the beginning and the end of the first and second courses of the therapy by two ophthalmologists. The results showed that the symptoms and signs were significantly improved in 33 (94.3%) cases. A decrease of eyeball protrusion of 1.22 +/- 1.15 and 1.28 +/- 1.15 mm in the left and right eyes respectively was shown by eophthalmometry reading (both P < 0.0005, compared with before and after the therapy). The decrease of exophthalmos was more remarkable in the cases with ophthalmopathy for < or = 1 year than that > 1 year. 11/22 patients recovered their ability to close eyes adequately. The diplopia was corrected in 8/15 cases. The mobility of eye ball returned to normal in 5/15 cases. Exposed lesion and/or ulceration of the cornea found in 7 patients were cured. Serious side and/or toxic effects of the drugs were not present during the course of therapy. It is suggested that DMPA regimen is an effective, safe and cheap approach to the treatment of Graves' ophthalmopathy.

Adult↗
PubMed1996

[Comparative analysis of clinical features of acute myocardial infarction in diabetic and non-diabetic patients].

We conducted match-control study to make a comparison between 20 diabetic and 20 non-diabetic patients in clinical features of acute myocardial infarction (AMI). There were 16 males and 4 females in each group. The mean age of diabetic group (DM) was 61.95 +/- 9.83 years, and that of non-diabetic group (NDM) was 61.45 +/- 9.38 years. We found the morbidity of silent myocardial infarction (MI) being 45% (DM) versus 10% (NDM); acute pulmonary edema being 40% (DM) versus 10% (NDM); cardiac shock, 35% (DM) versus 0% (NDM); arrhythmia, 70% (DM) versus 30% (NDM); the complication of cerebral infarction being 20% (DM) versus 0% (NDM); and complication of infection, 30% (DM) versus 10% (NDM). These revealed that DM had higher morbidity of silent MI and complications of AMI than NDM. Three diabetic patients had MI in two sites while one diabetic patient had myocardial remfarction, which showed DM had more serious damage in coronary artery than NDM. The mortality rate was 45% in DM and 15% in NDM. Multiple-organ functional failure was the main cause of death in DM.

Adult↗