Epstein-Barr virus-associated typical gastric carcinoma detected by in situ hybridization and polymerase chain reaction.
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Adenocarcinoma↗
Biomedical subjects
J J Lin
Publications and source records attributed to J J Lin.
Application of the polymerase chain reaction to monitor Mycobacterium tuberculosis DNA in the CSF of patients with tuberculous meningitis after antibiotic treatment.
The polymerase chain reaction (PCR) was used to detect Mycobacterium tuberculosis DNA in 29 CSF specimens from seven patients with tuberculous meningitis after the start of antituberculous chemotherapy. Ten of the 13 CSF specimens taken from these patients with an initial treatment of three weeks were positive for the PCR study. By contrast, only one of the other 16 CSF specimens taken from patients treated for more than three weeks was positive. This study shows that M tuberculosis DNA can exist in the CSF of a patient with tuberculous meningitis for three weeks after treatment and that PCR can still be a sensitive method to detect M tuberculosis DNA in the CSF after the start of treatment in patients with tuberculous meningitis.
Adolescent↗
Electrotransformation of Agrobacterium.
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Agrobacterium tumefaciens↗
Reporter genes and transient assays for plants.
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Chloramphenicol O-Acetyltransferase↗
Two isoforms of Drosophila dynamin in wild-type and shibire(ts) neural tissue: different subcellular localization and association mechanisms.
The temperature-sensitive mutations of the shibire (shi) gene in Drosophila cause endocytic arrest, resulting in neurotransmission block and paralysis at high temperatures. However, underlying mechanism for the defects is not yet known. We examined the subcellular distribution of dynamin, a product of the shi gene, by immunoblotting and immunocytochemical assays. Two isoforms of dynamin with apparent M(r) of 92 kD and 94 kD have been detected in wild-type and shi(n) adult neural tissue. The two isoforms were reproducibly associated with different subcellular fractions of head homogenates. The 94kD isoform is fractionated in the low speed (2.000 x g) pellet containing plasma membrane fragments, and the 92kD isoform in the high speed (130,000 x g) pellet. In this procedure, very little dynamin remained in the high speed supernatant fraction. The 94 kD isoform represents the majority (65-75%) of total dynamin and appears to be a peripheral membrane protein. It can be extracted from the low speed membrane pellet by high salt, Na2CO3 (pH 11) or Triton X-100 treatments. Extracted 94kD dynamin from both wild-type and mutant homogenates is able to reassociate with artificial phospholipid vesicles at both permissive and restrictive temperatures. Binding of the 94 kD dynamin to liposomes appears to be pH-dependent, varying most significantly within the physiological pH range, which may be functionally important. The 92 kD isoform cannot be released by high salt or Na2CO3 treatments and only a small fraction is released by Triton X-100, suggesting a different mechanism of association with cell structures. The distribution of the two isoforms is not altered by the presence of stabilized microtubules in homogenates. No apparent degradation or subcellular redistribution of mutant dynamin was detected in two shi(n) alleles after heat shock or block of the dynamin GTPase activity, suggesting that intracellular redistribution or degradation of mutant dynamin are not involved in the endocytosis arrest in these mutants. These observations resemble the effect of endocytosis arrest by GTP-gamma-S in rat brain synaptosomes (Takei et al., 1995), in which dynamin is trapped at the neck of invaginated pits but is absent in the clathrin-coated distal end undergoing internalization. Our finding that endocytosis arrest by shi(n) mutations and GTP-gamma-S do not lead to cumulation of dynamin in the low speed pellet fraction further suggests that the 94 kD isoform remains associated with the plasma membrane during coated vesicle pinch-off and that the two isoforms do not appear to correspond to different functional states of dynamin but are likely to be involved in separate cellular compartments within the membrane cycling pathway (e.g., the plasma membrane, endosomes, and endoplasmic reticulum).
Amino Acid Sequence↗
Insulin-like growth factor-1 enhances epidermal growth factor receptor activation and renal tubular cell regeneration in postischemic acute renal failure.
Growth factors such as insulin-like growth factor-1 (IGF-1), epidermal growth factor (EGF), and hepatocyte growth factor have been shown to accelerate the recovery from postischemic acute renal failure (ARF) with a concomitant increase in DNA synthesis. Interactions between growth factors have been demonstrated in a number of in vitro studies. This study examined the effect of exogenous IGF-1 on the DNA synthesis and EGF receptor (EGF-R) activation in postischemic rat kidneys. Thirty minutes after the relief of 30-minute total occlusion of the left renal artery in anesthetized 225 to 300 gm Sprague-Dawley rats, either IGF-1 (75 micrograms/kg) or normal saline solution (NS, 0.2 ml) was given by intravenous bolus, followed by twice daily subcutaneous injections of IGF-1 (50 micrograms/kg) or 0.2 ml NS for 4 days, respectively, in IGF-1-Tx) and NS treated (NS-Tx) groups (n = 8 each). On the day after the completion of treatment, inulin clearance (ml/kg/min) of the postischemic kidneys in the IGF-1-Tx group was significantly higher (p < 0.01) than inulin clearance of kidneys in the NS-Tx group. This was associated with improved kidney morphology. IGF-1 treatment also enhanced the labeling index of 5-bromo-2'-deoxyuridine (percent of stained tubule cells), a marker for active DNA synthesis, in the outer medulla of postischemic kidneys at 1 day and 2 days after the injury. EGF-R tyrosine phosphorylation (which reflects receptor activation) increased in postischemic kidneys in both NS-Tx (n = 5) and IGF-1-Tx (n = 3) groups 1 day after the injury as compared with nonischemic contralateral kidneys. In the IGF-1-Tx group there was also increased iodine 125-labeled EGF binding and EGF-R protein. Our results demonstrate a beneficial effect of IGF-1 on postischemic ARF. Furthermore, they suggest that EGF-R activation is involved in tubular regeneration and that IGF-1 may enhance EGF-R activation by increasing EGF-R expression.
Acute Kidney Injury↗
A young adult with tuberculous meningitis diagnosed by polymerase chain reaction on serial CSF samples: a case report.
A polymerase chain reaction (PCR) assay was used to diagnose a young adult with tuberculous meningitis who presented with unusual clinical symptoms of an acute illness. He had repeated cerebrospinal fluid (CSF) samples taken, and the PCR assay for detecting mycobacterial deoxyribonucleic acid was negative for the first two CSF specimens, but was positive in the third. He was then treated with antituberculous drugs and had complete restoration three months later. A follow-up PCR of the CSF was still positive after one month of therapy using antituberculous drugs, but converted to a negative result one month later. It is concluded that it is valuable to repeatedly sample CSF specimens for PCR study in patients with clinically suspected tuberculous meningitis.
Adult↗
Vertebral artery dissection complicated by cervical manipulation: a case report.
A 32-year-old healthy man developed vomiting, blurred vision, and consciousness disturbance following cervical manipulation. Physical examination showed stuporous consciousness and spontaneous horizontal nystagmus. Computed tomography (CT) and magnetic resonance (MR) imaging of the brain revealed infarction in the territory of the basilar artery. Studies of MR angiography and vertebral angiography disclosed dissection of the right vertebral artery at the atlantoaxial segment. Antiedematous drugs were prescribed and the patient gradually improved. Neurologic examination six months later demonstrated mild cerebellar ataxia. Physicians and patients should be aware that vertebro-basilar dissection may follow cervical manipulation, and, more importantly, should attempt to prevent progressive infarction.
Adult↗
Hemiballism-hemichorea: clinical study in 23 Chinese patients.
BACKGROUND: Hemiballism-hemichorea, a well documented movement disorder, is not uncommon in the clinic. However, systematic analysis of the condition in ethnic Chinese on clinical grounds, is still inexplicably lacking. METHODS: This study focused on 23 Chinese patients with hemiballism-hemichorea in Taiwan. The general data, clinical pictures, blood biochemistries, past histories of systemic disease, neuroradiological imaging, methods of treatment, and prognoses of these patients were analyzed retrospectively. RESULTS: The study revealed that ischemic stroke (44%) is the leading cause of this movement disorder, and the metabolic disorder (22%) is also one of the common etiologies of dyskinesia in Chinese patients. In addition to those patients whose condition was caused by non-ketotic hyperglycemia, blood sugar had also obviously increased in patients where the cause was infarction. Pathological lesions contributed to hyperkinesia were found not only in the contralateral basal ganglion but also in the thalamus and subcortical areas. The characteristics of those patients where the cause was infarction and non-ketotic hyperglycemia were: age at onset greater than 60 years, and predominantly in women. Etiologies contributing to this movement disorder in younger patients differ from those in the older. Prognosis of the movement disorder in this study was favorable. CONCLUSIONS: Hemiballism-hemichorea is predisposed to occur in older Chinese women, and metabolic disorder is an important etiology of the movement disorder. When the dyskinesia is encountered in the clinic, the metabolic disorders must be first ruled out as the problem may be rapidly resolved by achieving metabolic control.
Adolescent↗
Peritoneal transport in type I (insulin-dependent) and type II (noninsulin-dependent) diabetic peritoneal dialysis patients.
Alterations in the fibrinolytic system have been demonstrated in noninsulin-dependent diabetic patients (NIDDM) but not in insulin-dependent diabetic patients (IDDM). Since the activity of the fibrinolytic system can affect the turnover of extracellular matrix and therefore theoretically can affect the peritoneal transport, we tried to determine if there was a difference in the performance of the peritoneal equilibration test (PET) between IDDM and NIDDM patients receiving peritoneal dialysis (PD). The PET data from 11 IDDM patients (2 female, 9 male) and 13 NIDDM patients (3 female, 10 male) were reviewed. These two groups of patients were matched in gender, duration of end-stage renal disease, PD, and hypertension, blood pressure, degree of uremia, weekly KT/V, and body surface area. The IDDM patients (41.4 +/- 13.9 years) were younger than the NIDDM patients (58.8 +/- 7.1 years, p = 0.0026). There were no differences in hematocrit and serum chemistry profile including glucose and albumin between the two groups. Our data showed that there was no difference in PET performance between IDDM and NIDDM patients.
Adult↗
Increased peritoneal solute transport in diabetic peritoneal dialysis patients.
Microangiopathy has been observed in the peritoneum of diabetic patients, and an increase in vascular permeability to small and large molecules has been described in the skeletal muscle of diabetic patients. Therefore, we examined the peritoneal equilibration test (PET) data from 19 diabetic and 19 nondiabetic stable peritoneal dialysis (PD) patients. These two groups of patients were matched in terms of age, gender, duration of PD and hypertension, incidence of peritonitis, levels of blood pressure, degree of uremia, levels of serum lipids, hematocrit, weekly KT/V, and body surface area. Compared to the nondiabetics, the diabetics had higher dialysate-to-serum ratios or mass transfer coefficients of urea or creatinine. These differences were not related to their differences in serum sodium or glucose. Regression analysis showed that the duration of hypertension was a negative determinant of peritoneal transport of urea and creatinine in diabetic patients. Our results suggest that the diabetic patients had a higher peritoneal diffusive transport of small solutes, which was offset by their duration of hypertension.
Biological Transport↗
Plasminogen activator inhibitor-1 and peritoneal transport in diabetic and non-diabetic peritoneal dialysis patients.
Plasminogen activator inhibitor-1 (PAI-1) is an important regulator of plasminogen activators and has been shown to be involved in the accumulation of extracellular matrix (ECM) in various tissues. Since peritoneal interstitium is one of the main resistance sites of peritoneal transport, the level of PAI-1 in the peritoneum may have a significant effect on water and solute transport during peritoneal dialysis (PD) via its effect of peritoneal ECM. Therefore, we studied the associations between plasma or dialysate PAI-1 levels and the peritoneal transport during standard peritoneal equilibration test (PET) in 8 diabetic and 8 non-diabetic stable PD patients who were matched for their demographical data. There were no differences in plasma PAI-1 levels and PET variables between these two groups of patients. In each group, there was an increase in dialysate PAI-1 level with dwell time as a result of the diffusion of plasma PAI-1 into peritoneal cavity and the local production and release of PAI-1 in peritoneal tissue. However, the extent of this increase was less in the former. In non-diabetic patients, the change in dialysate PAI-1 amount was a significant positive predictor for the diffusive transports of urea and transport. These results are consistent with the hypothesis that peritoneal PAI-1 has a significant effect on peritoneal transport during PD. Further studies including more patients are needed to confirm our observations, and studies providing more direct evidence are needed to test this hypothesis.
Biological Transport↗
Characterization of cis-regulating elements and trans-activating factors of the rat cardiac troponin T gene.
To study the transcriptional regulation of the rat cardiac troponin T (cTnT) gene, chimeric genes composed of the upstream region (-757 to +193 base pairs (bp) relative to the transcription initiation site) of the cTnT gene and the bacterial chloramphenicol acetyltransferase (CAT) gene were constructed and transfected into primary cultures of neonatal cardiomyocytes and cardiac fibroblasts. Deletion analysis showed that a 41-bp fragment (-249 to -209 bp) containing the MEF-2-like motif is an essential element for minimal cardiac-specific expression of the rat cTnT gene. The proximal promoter (-208 to -1 bp) contains two consensus CArG boxes, one M-CAT motif, one AP2 site, and one TATA box. The construct (cTNT-208) composed of the CAT reporter gene driven by this proximal promoter did not show cardiac muscle-specific expression. Ligation of consensus MEF-2-like sequence into the upstream of this chimera only partially increased its ability to express in cardiomyocytes. These results suggest that the spacing among MEF-2-like motif and proximal promoter and/or the flanking sequences of the MEF-2-like motif are important in determining cardiac muscle-specific expression. By footprint analysis with a DNA fragment (-303 to +6 bp), we identified three novel regions (called A, B, and C) protected by protein extract from rat hearts, in addition to the known motifs such as MEF-2, M-CAT, and CArG. Gel retardation with the probe (-235 to -141 bp), containing the MEF-2-like motif, one of the CArG boxes, and the C region, or the 41-bp probe (-249 to -209 bp), containing the MEF-2-like motif, revealed different DNA-protein complexes formed by heart, skeletal muscle, and liver extracts. By using DNA affinity purification, DNA-binding proteins with apparent molecular masses of 22-26 kDa were identified from rat heart extract but not from skeletal and liver extracts, suggesting the involvement of cardiac-specific proteins in regulating the cTnT gene expression.
Animals↗
Isolation and characterization of two Saccharomyces cerevisiae genes that encode proteins that bind to (TG1-3)n single strand telomeric DNA in vitro.
By screening lambda gt11 libraries with a radiolabeled (TG1-3)n oligonucleotide, two Saccharomyces cerevisiae genes were identified that encode polypeptides that recognize the single-stranded telomeric repeat sequence (TG1-3)n. The first gene, NSR1, a previously identified gene, encodes a protein involved in ribosomal RNA maturation and possibly in transport of proteins into the nucleus. The second gene, GBP2 (G-strand Binding Protein), is an anonymous open reading frame from chromosome III. These two genes contain RNA recognition motifs (RRMs) that are found in proteins that interact with RNA. Both Nsr1p and Gbp2p bind specifically to yeast single strand (TG1-3)n DNA in vitro. To test whether these two proteins associate with telomeres in vivo, strains were constructed in which one or both of these genes were either disrupted or overexpressed. None of these alterations affected telomere length or telomere position effect. The potential role of these two (TG1-3)n binding proteins is discussed.
Base Sequence↗
Characterization of the mechanism of cellular and cell free protein synthesis inhibition by an anti-tumor ribonuclease.
Onconase, a protein with anti-tumor activity, causes potent inhibition of protein synthesis in the rabbit reticulocyte lysate (IC50 10(-11) M) and when microinjected into Xenopus oocytes (IC50 10(-10) M). Onconase is a member of the RNase A superfamily; however, unlike RNase A, the mechanism of protein synthesis inhibition does not involve apparent degradation of lysate or cellular ribosomal RNAs. Rather, reticulocyte and oocyte tRNA is hydrolyzed after Onconase treatment. Furthermore, re-addition of tRNA to Onconase pretreated lysates or oocytes restores the translational capacity of the system. Taken together these results suggest that Onconase causes potent protein synthesis inhibition by a mechanism involving inactivation of cellular tRNA.
Animals↗
Erythrocyte tropomodulin binds to the N-terminus of hTM5, a tropomyosin isoform encoded by the gamma-tropomyosin gene.
Tropomodulin is a 40.6-kDa protein that binds to one end of the rod-like tropomyosin and inhibits its cooperativity and binding to actin. In myofibrils, tropomodulin has been localized at or near the free end of thin filaments. Using recombinant and chimeric molecules in a solid-phase binding assay, we demonstrate that it is the N-terminus of tropomyosin that interacts with tropomodulin. Among several tropomyosin isoforms tested, hTM5 encoded by the human gamma-tropomyosin gene has the highest affinity toward human erythrocyte tropomodulin. Tropomodulin may, therefore, regulate the length and/or organization of actin filaments by differential binding to tropomyosin isoforms. hTM5 exists in the human erythrocyte membrane skeleton. In non-muscle cells, tropomodulin may block the head-to-tail association of tropomyosins and their interaction with actin at the pointed end of actin filaments by preferentially binding to TM5 at its N-terminus.
Actins↗
Overexpression of human fibroblast caldesmon fragment containing actin-, Ca++/calmodulin-, and tropomyosin-binding domains stabilizes endogenous tropomyosin and microfilaments.
Fibroblast caldesmon is a protein postulated to participate in the modulation of the actin cytoskeleton and the regulation of actin-based motility. The cDNAs encoding the NH2-terminal (aa.1-243, CaD40) and COOH-terminal (aa.244-538, CaD39) fragments of human caldesmon were subcloned into expression vectors and we previously reported that bacterially produced CaD39 protein retains its actin-binding properties as well as its ability to enhance low M(r) tropomyosin (TM) binding to actin and to inhibit TM-actin-activated HMM ATPase activity in vitro (Novy, R. E., J. R. Sellers, L.-F. Liu, and J. J.-C. Lin. 1993. Cell Motil. Cytoskeleton. 26:248-261). Bacterially produced CaD40 does not bind actin. To study the in vivo effects of CaD39 expression on the stability of actin filaments in CHO cells, we isolated and characterized stable CHO transfectants which express varying amounts of CaD39. We found that expression of CaD39 in CHO cells stabilized microfilament bundles as well as endogenous TM. CaD39-expressing clones displayed an increased resistance to cytochalasin B and Triton X-100 treatments and yielded increased amounts of TM-containing actin filaments in microfilament isolation procedures. In addition, analysis of these clones with immunoblotting and indirect immunofluorescence microscopy with anti-TM antibody revealed that stabilized endogenous TM and enhanced TM-containing microfilament bundles parallel increased amounts of CaD39 expression. The increased TM observed corresponded to a decrease in TM turnover rate and did not appear to be due to increased synthesis of endogenous TM. Additionally, the phenomenon of stabilized TM did not occur in stable CHO clones expressing CaD40. Therefore, it is likely that CaD39 can enhance TM's binding to F-actin in vivo, thus reducing TM's rate of turnover and stabilizing actin microfilament bundles.
Actin Cytoskeleton↗
Hemiballism-hemichorea and non-ketotic hyperglycaemia.
Three patients with hemiballism-hemichorea caused by non-ketotic hyperglycaemia are presented, two of whom had hyperosmolar non-ketotic hyperglycaemic syndrome. In two of the three patients, the hyperkinesia was the initial presenting symptom of their diabetes mellitus. The hypersensitivity of the postmenopausal dopamine receptor, decreased gamma-aminobutyric acid in the brain in non-ketotic hyperglycaemia, coexisting lacunar infarct in the basal ganglion, and pre-existing metabolic dysfunction in the basal ganglion may all have played a part in the pathogenesis of this movement disorder.
Aged↗