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Biomedical subjects

J Tong

Publications and source records attributed to J Tong.

At least 127 records · Page 7Linked to original sources
PubMed1991

In vitro response of T cells from aplastic anemia patients to antilymphocyte globulin and phytohemagglutinin: colony-stimulating activity and lymphokine production.

The aim of the present study was to compare the response of bone marrow (BM) lymphocytes from patients with aplastic anemia (AA) or normal controls to increasing doses of antilymphocyte globulin (ALG) or phytohemagglutinin (PHA). For this purpose BM T-enriched cells from 11 AA patients and 9 normal individuals were incubated with ALG (0-1000 micrograms/ml) or PHA (0%-10%) for 1 day, and the supernatants were tested for suppression/enhancement of granulocyte-macrophage colony-forming unit (CFU-GM) growth and for release of granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) assayed with the enzyme-amplified sensitivity immunoassay (EASI). The production of colony-stimulating activity (CSA) by T cells primed with ALG and tested in the absence of exogenous GM-CSF correlated with the dose of ALG in priming cultures up to 14% EG (100% EG = CFU-GM growth with 30 ng/ml of GM-CSF). The amount of GM-CSF in the supernatants paralleled their capacity to sustain CFU-GM growth (up to 3.5 ng/ml of GM-CSF). Production of CSA or GM-CSF from T cells primed with PHA was significantly lower. Supernatants of PHA-primed T cells, when added to normal BM cells in the presence of exogenous GM-CSF, produced a dose-dependent inhibition of CFU-GM growth (down to 13% +/- 10% EG). The same supernatants contained detectable amounts of IFN-gamma and TNF-alpha (21 +/- 6.7 IU/ml and 4.6 +/- 2.9 ng/ml, respectively). IFN-gamma production from severe AA (SAA) T cells in response to PHA was significantly superior to the IFN-gamma production from normal T cells (21 +/- 6.7 IU/ml vs 9.5 +/- 7.1 IU/ml, p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Long-term effects of physiologic concentrations of dexamethasone on human bone-derived cells.

Bone cells derived from human trabecular explants display osteoblastic features. We examined the modulation of alkaline phosphatase activity and cAMP production as the result of exposing trabecular explants to physiologic concentrations of dexamethasone for 4 weeks during cellular outgrowth and subculture. Cells treated with dexamethasone were observed to grow generally more slowly than control cells. Cells appeared larger and more polygonal, and staining for alkaline phosphatase was more intense in the dexamethasone-exposed cultures. There was a progressive increase in cellular PTH responsiveness with increasing duration of exposure of cells to dexamethasone. Cells grown for 6 weeks in 3 x 10(-8) M dexamethasone had a 10-fold increase in PTH-stimulated cyclic AMP accumulation. Dexamethasone-treated cells also had a significantly increased alkaline phosphatase activity. 1,25-(OH)2D3-stimulated alkaline phosphatase activity was increased approximately 20-fold. cAMP responses were significantly increased to PTH (21.7-fold), PGE1 (2.67-fold), and forskolin (4.81-fold), but not to cholera toxin. Dexamethasone-treated cells also had a mean decrease in 1,25-(OH)2D3-stimulated osteocalcin production to 26.2% of control values (p less than 0.001). Hydrocortisone treatment gave rise to similar effects but of smaller magnitude than those of dexamethasone. Testosterone did not have a significant effect on alkaline phosphatase activity or cAMP production. Skin fibroblasts showed a significant enhancement of alkaline phosphatase activity in response to dexamethasone, but of a much smaller magnitude than in bone cells. The phenotypic changes induced by long-term culture in dexamethasone are consistent with the promotion of a more differentiated osteoblastic phenotype.

Adenylyl Cyclases↗
PubMed1990

Cyclosporin A and chronic graft versus host disease.

One hundred and seventeen patients undergoing allogeneic bone marrow transplantation (BMT) for severe aplastic anemia (n = 18) or leukemia (n = 99) who were alive on day +180, were analysed for the incidence and severity of chronic graft-versus-host disease (cGVHD), developing before or after discontinuation of cyclosporin A (CSA). All patients received CSA for GVHD prophylaxis for 94 to greater than 988 days post-BMT. cGVHD developed in 74 patients (63%) before CSA discontinuation (de novo n = 12, progression from acute GVHD n = 42, following resolution of acute GVHD n = 20). CSA was discontinued in 112 patients: electively (n = 80), because of toxicity (n = 8), or following relapse of leukemia (n = 24). In five patients CSA was never discontinued. After discontinuation of CSA, progression or de novo cGVHD was seen in 25 patients, with a significant difference in patients treated for more or less than 150 days (8% vs 41%, p = 0.0007). In 15 patients CSA had to be re-instituted and in 14 it could be discontinued a second time. Overall 111/117 (94%) patients have finally discontinued CSA. In conclusion cGVHD will progress or appear de novo in 41% of patients receiving CSA for less and in 8% of those receiving CSA for more than 150 days respectively, indicating that the drug should be administered for at least 5 months post-BMT. Most patients (94%) will eventually become CSA independent.

Adolescent↗
PubMed1989

Effect of antilymphocyte globulin (ALG) on bone marrow T/non-T cells from aplastic anaemia patients and normal controls.

UNLABELLED: The aim of this study was twofold: (a) to test the effect of antilymphocyte globulin (ALG) on bone marrow (BM) T/non-T cells, and (b) to look for a possible differential response of cells from severe aplastic anaemia (SAA) patients and controls. For this purpose bone marrow T/non-T cells from normal individuals (n = 7) or aplastic patients (SAA, n = 13) were kept in liquid culture with or without ALG. Supernatants were then tested for enhancement/suppression on colony forming unit, granulocyte-macrophage (CFU-GM) growth (in the presence of exogenous recombinant granulocyte-macrophage colony stimulating factor (rGM-CSF)), or for their ability to support CFU-GM growth (in the absence of exogenous rGM-CSF). Supernatants from SAA T cells suppressed CFU-GM growth of normal bone marrow cells in 5/12 patients (mean expected growth (EG) 71 +/- 16%), but not after incubation with ALG (mean 110 +/- 29% EG, P = 0.03). No inhibition could be obtained with the supernatants from untreated normal T cells. Significant enhancement was seen with ALG treated versus untreated SAA T cells (142 +/- 28% EG v. 105 +/- 61% EG, P = 0.01) and with ALG treated versus untreated SAA non-T cells (165 +/- 26% EG v. 105 +/- 23% EG, P = 0.01), but not in controls. Supernatants from SAA and control T/non-T cells were capable of promoting colony formation in the absence of rGM-CSF (colony-stimulating activity (CSA) production): 16 +/- 14% for SAA-T cells and 19 +/- 18% EG for non-T cells (100% = 30 ng rGM-CSF/ml). The addition of ALG increased CSA production in T cells to 37 +/- 23% EG (P = 0.04) and in non-T cells to 40 +/- 13% EG (P = 0.04). Similar results could be obtained in controls. IN CONCLUSION: (a) ALG interacts in vitro with bone marrow T and non-T cells from SAA patients, down-regulating the production of negative lymphokines and enhancing the release of haemopoietins; (b) the latter, but not the former effect, can be shown also with cells from normal controls. The two effects are not mutually exclusive, and are likely to provide maximal benefit in vivo.

Anemia, Aplastic↗
PubMed1988

Adenovirus type 12 E1B 19-kilodalton protein is not required for oncogenic transformation in rats.

The adenovirus type 12 mutants in700 and pm700 carry site-specific mutations within the reading frame encoding the E1B 19-kilodalton protein (19K protein) which prevent the production of the intact 19K protein. In cultures of human A549 cells, these mutants grow just as well as the wild-type virus does, but they display a large-plaque (lp), cytocidal (cyt) phenotype. DNA in these infected cells is not degraded, but at late times in human KB cells infected by the mutants, the mutants display a DNA degradation (deg) phenotype. The transformation phenotype of these mutants is also host range. Although the mutants are defective for transformation of the 3Y1 rat cell line, they transform rat and mouse primary kidney cells in vitro at wild-type efficiency and are capable of inducing tumors in rats. These results support the view that the type 12 E1B 19K protein is not obligatory for oncogenic transformation.

Adenovirus Early Proteins↗
PubMed1987

Changes in the levels of translatable glutaminase mRNA during onset and recovery from metabolic acidosis.

The amount of the mitochondrial glutaminase present within rat kidney is increased 5-fold during chronic metabolic acidosis. This adaptive response is due to a corresponding increase in the relative rate of glutaminase synthesis. Poly(A+) RNA was purified from the kidneys of control, 7-day acidotic, and 2-day recovered rats and then fractionated by electrophoresis on a low melting temperature agarose gel. Translation of the fractionated RNA in a rabbit reticulocyte lysate yields a 72,000-dalton protein that is specifically precipitated by anti-glutaminase IgG. The level of this protein is at least 3-fold greater in the translation products of the fractionated poly(A+) RNA derived from the acidotic vs. control or recovered rats. Therefore, the 72,000-dalton product of translation is the apparent precursor to the 68,000- and 65,000-dalton proteins that are contained in the mitochondrial glutaminase. From its relative electrophoretic mobility, the size of the glutaminase mRNA was estimated to be approximately 6.5 kilobases. The relative levels of translatable glutaminase mRNA were determined by using unfractionated poly(A+) RNA prepared from rats at various times following onset and recovery from acidosis. The observed increase occurred gradually, requiring 7 days to reach a maximal induction of 4.2-fold. The increase could be due to the increased transcription of a stable mRNA (t1/2 approximately 3 days). However, 2 days of recovery was sufficient to return the level of translatable glutaminase mRNA to normal. Thus, the selective inactivation or the altered stability of the glutaminase mRNA must also contribute to the regulation of the glutaminase gene expression.

Acidosis↗
PubMed1986

The effect of metabolic acidosis on the synthesis and turnover of rat renal phosphate-dependent glutaminase.

Regulation of the mitochondrial phosphate-dependent glutaminase activity is an essential component in the control of renal ammoniagenesis. Alterations in acid-base balance significantly affect the amount of the glutaminase that is present in rat kidney, but not in brain or small intestine. The relative rates of glutaminase synthesis were determined by comparing the amount of [35S]methionine incorporated into specific immunoprecipitates with that incorporated into total protein. In a normal animal, the rate of glutaminase synthesis constitutes 0.04% of the total protein synthesis. After 7 days of metabolic acidosis, the renal glutaminase activity is increased to a value that is 5-fold greater than normal. During onset of acidosis, the relative rate of synthesis increases more rapidly than the appearance of increased glutaminase activity. The increased rate of synthesis reaches a plateau within 5 days at a value that is 5.3-fold greater than normal. Recovery from chronic acidosis causes a rapid decrease in the relative rate of glutaminase synthesis, but a gradual decrease in glutaminase activity. The former returns to normal within 2 days, whereas the latter requires 11 days. The apparent half-time for glutaminase degradation was found to be 5.1 days and 4.7 days for normal and acidotic rats respectively. These results indicate that the increase in renal glutaminase activity associated with metabolic acidosis is due primarily to an increase in its rate of synthesis. From the decrease in activity that occurs upon recovery from acidosis, the true half-life for the glutaminase was estimated to be 3 days.

Acidosis↗
PubMedDate not supplied

Comparison of laparoscopic total and partial fundoplication for gastroesophageal reflux.

Approximately 25% of patients with gastroesophageal reflux severe enough to be considered for surgical treatment have dysfunction of esophageal peristalsis in addition to dysfunction of the lower esophageal sphincter. A standard total (i.e., Nissen) fundoplication in these patients may be followed by dysphagia, so many experts recommend a partial fundoplication as an alternative. The goal of this study was to compare the clinical results and changes in esophageal function following laparoscopic total and partial fundoplication. Ninety-three patients with gastroesophageal reflux disease had laparoscopic antireflux operations. Total fundoplication was performed in 50 patients with normal esophageal peristalsis. Partial fundoplication was chosen for 43 patients with severe abnormalities of esophageal peristalsis. The same percentage of patients has resolution of heartburn (93%) and regurgitation (97%) after partial as compared to total fundoplication. Dysphagia developed in four patients (8%) after total fundoplication (one patient required dilatation) and in no patients after partial fundoplication. Both operations produced similar changes in lower esophageal sphincter function, but only partial fundoplication was associated with improvement in esophageal dysfunction. Esophageal acid exposure became normal in 92% of patients after total and in 91% of patients after partial fundoplication. Partial fundoplication improves lower esophageal sphincter pressure and esophageal body function and, in patients with abnormal esophageal peristalsis, it corrects reflux without producing dysphagia. Partial and total fundoplication are both indicated in patients with gastroesophageal reflux disease, and the choice of which procedure to use should be based on each patient"s specific esophageal motor function abnormalities.

Deglutition Disorders↗
PubMedDate not supplied

Importance of preoperative and postoperative pH monitoring in patients with esophageal achalasia.

Gastroesophageal reflux (GER) can develop in patients with esophageal achalasia either before treatment or following pneumatic dilatation or Heller myotomy. In this study we assessed the value of pre- and postoperative pH monitoring in identifying GER in patients with esophageal achalasia. Ambulatory pH monitoring was performed preoperatively in 40 patients with achalasia (18 untreated patients and 22 patients after pneumatic dilatation), 27 (68%) of whom complained of heartburn in addition to dysphagia (group A), and postoperatively in 18 of 51 patients who underwent a thoracoscopic (n=30) or laparoscopic (n=21) Heller myotomy (group B). The DeMeester reflux score was abnormal in 14 patients in group A, 13 of whom had been treated previously by pneumatic dilatation. Two types of pH tracings were seen: (1) GER in eight patients (7 of whom had undergone dilatation) and (2) pseudo-GER in six patients (all 6 of whom had undergone dilatation). Therefore 7 (32%) of 22 patients had abnormal GER after pneumatic dilatation. Postoperatively (group B) seven patients had abnormal GER (6 after thoracoscopic and 1 after laparoscopic myotomy). Six of the seven patients were asymptomatic. These findings show that (1) approximately one third of patients treated by pneumatic dilatation had GER; (2) symptoms were an unreliable index of the presence of abnormal GER, so pH monitoring must be performed in order to make this diagnosis; and (3) the preoperative detection of GER in patients with achalasia is important because it influences the choice of operation.

Adult↗
PubMedDate not supplied

Comparison of thoracoscopic and laparoscopic Heller myotomy for achalasia.

For more than three decades experts have debated the relative merits of thoracoscopic Heller myotomy (no antireflux procedure) vs. laparoscopic Heller myotomy plus Dor fundoplication for treatment of achalasia. The aim of this study was to compare the results of these two methods with respect to (1) relief of dysphagia, (2) incidence of postoperative gastroesophageal reflux, and (3) hospital course. Sixty patients with esophageal achalasia were operated on between 1991 and 1996. Thirty underwent a thoracoscopic Heller myotomy and 30 had a laparoscopic Heller myotomy with a Dor fundoplication. The two groups were similar with respect to demographic characteristics, clinical findings, and extent of manometric abnormalities. Preoperative pH monitoring showed abnormal reflux in two patients in the laparoscopic group. Average hospital stay was 84 hours for the thoracoscopic group and 42 hours for the laparoscopic group. Excellent (no dysphagia) or good (dysphagia less than once a week) results were obtained in 87% of patients in the thoracoscopic group and in 90% of patients in the laparoscopic group. Postoperative pH monitoring showed abnormal reflux in 6 (60%) of 10 patients in the thoracoscopic group and in 1 (10%) of 10 patients in the laparoscopic group. The two patients in the laparoscopic group who had reflux preoperatively had normal reflux scores postoperatively. Laparoscopic Heller myotomy with Dor fundoplication was found to be superior to thoracoscopic Heller myotomy. Both operations relieved dysphagia, but the laparoscopic approach avoided postoperative reflux and even corrected reflux present preoperatively. In addition, the patients were more comfortable and left the hospital earlier following a laparoscopic myotomy. Whether it is truly possible to perform a Heller myotomy without an antireflux procedure in a way that relieves dysphagia and regularly avoids reflux remains questionable.

Adult↗
PubMedDate not supplied

Active sliding between cytoplasmic microtubules.

Microtubules are versatile cellular polymers that play a role in cell shape determination and mediate various motile processes such as ciliary and flagellar bending, chromosome movements and organelle transport. That a sliding microtubule mechanism can generate force has been demonstrated in highly ordered structures such as axonemes, and microtubule-based force generation almost certainly contributes to the function of mitotic and meiotic spindles. Most cytoplasmic microtubule arrays, however, do not exhibit the structural regularity of axonemes and some spindles, and often appear disorganized. Yet many cellular activities (such as shape changes during morphogenesis, axonal extension and spindle assembly) involve highly coordinated microtubule behaviour and possibly require force generated by an intermicrotubule sliding mechanism, or perhaps use sliding to move microtubules rapidly into a protrusion for stabilization. Here we show that active sliding between cytoplasmic microtubules can occur in microtubule bundles of the amoeba Reticulomyxa. A force-producing mechanism of this sort could be used by this organism to facilitate the extension of cell processes and to generate the dynamic movements of the cytoplasmic network.

Adenine↗
PubMedDate not supplied

The change of C-fos expression in ovariectomized rats following electroacupuncture treatment--an immunohistochemistry study.

The roles of electroacupuncture (EA) in regulating the function of ovulation in rat have been investigated; however, the systematic study for the involvement of neural population of central nervous system (CNS) in acupuncturing the ovariectomized rat for promoting functional recovery has not been well understood. The present research was designed to examine, by C-fos immunocytochemistry, the distribution of Fos labelled neuron in CNS after acupuncturing the point of "Zhong-Ji (RN3)", "Guan-Yuan (RN4)", "San-Ying-Jiao (SP6)" and "Zi-Gong (EXCA1)" in ovariectomized rat. The area occupied by Fos protein labelled neuron, two hours after ovariotomy, was detected in medial preoptic nucleus (MPN), lateral preoptic nucleus (LPN), suprachiasmatic nucleus (SCN), paraventricular nucleus of the hypothalamus (PANH), medial amygdala nucleus (MAN), periventricular nucleus of the hypothalamus (PVNH), ventromedial nucleus of the hypothalamus (VNH), and arcuate nucleus (AR). The C-fos immunoreactive labelled neurons disappeared two weeks later following ovariotomy. The rat, recovering for two weeks after ovariotomy, received EA, and many specific Fos labelled cell were observed in LPN, PVNH, VNH, SCN and especially in AR, PANH and MPN, but not any labelled neuron could be found in MAN. No obvious C-fos expression was shown in these areas in the control group and EA group without ovariotomy. These results indicate that the above structures involved in regulating the function of hypothalamus-pituitary-ovarian axis and EA could modulate this function through effects on the above nuclei.

Animals↗
PubMedDate not supplied

[An autopsy case of Ehlers-Danlos syndrome showing various types of cerebrovascular disease].

We report a 73-year-old woman with Ehlers-Danlos syndrome (EDS) and hypertension who had developed various types of cerebrovascular disease. She had suffered from cerebral hemorrhage of the left putamen at the age of 58, of the left parietal lobe at 64 and cerebral infarction of right internal capsule at 71. EDS type II or III was suggested by two times of skin biopsies. A brain CT at the age of 73 revealed a comparatively large cerebral aneurysm in the territory of the anterior cerebral artery. The patient was treated conservatively, but died due to rupture of the aneurysm. The wall of the aneurysm was made up thin collagen fibers without elastic fibers. There were other multiple small aneurysms in the cerebral arteries, but none in other organs. Deposition of acid mucopolysaccharides was noted in the media of the abdominal aorta. Finally, the present case was thought most likely to be of EDS type IV. It was suggested that one of the causes of the cerebral hemorrhage at the ages of 58 and 64 and the infarction at 71 was related to hypertension, since brain MR angiography at 71 showed no clear aneurysms. In cases of EDS, one should consider the possible formation or rupture of cerebral aneurysm even though the course is favorable.

Aged↗