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Biomedical subjects

L Baker

Publications and source records attributed to L Baker.

At least 73 records · Page 4Linked to original sources
PubMed1996

Children's methods of coping with stress: a twin study of genetic and environmental influences.

The relative importance of environmental and hereditary factors in how children cope with stress was examined. Emotion-focused, problem-focused, and additional coping variables were assessed in 44 monozygotic (MZ) and 30 dizygotic (DZ) twin pairs, aged 9-16 years. The effects of heritability, shared environment, and unshared environment were examined in structural modelling analyses. Genetic factors accounted for a majority of the reliable variance in four of seven coping variables, while effects of twins' shared environment were negligible for all but one coping variable. Environmental factors important to individual differences in coping strategies were primarily unique to each child (unshared between the twins), highlighting the importance of individual experiences in shaping coping behaviors.

Adaptation, Psychological↗
PubMed1995

Selective trafficking of KNOTTED1 homeodomain protein and its mRNA through plasmodesmata.

Plasmodesmata are intercellular organelles in plants that establish cytoplasmic continuity between neighboring cells. Microinjection studies showed that plasmodesmata facilitate the cell-to-cell transport of a plant-encoded transcription factor, KNOTTED1 (KN1). KN1 can also mediate the selective plasmodesmal trafficking of kn1 sense RNA. The emerging picture of plant development suggests that cell fate is determined at least in part by supracellular controls responding to cellular position as well as lineage. One of the mechanisms that enables the necessary intercellular communication appears to involve transfer of informational molecules (proteins and RNA) through plasmodesmata.

Amino Acid Sequence↗
PubMed1995

Human fructose-1,6-bisphosphatase gene (FBP1): exon-intron organization, localization to chromosome bands 9q22.2-q22.3, and mutation screening in subjects with fructose-1,6-bisphosphatase deficiency.

Fructose-1,6-bisphosphatase (EC 3.1.3.11) is a key regulatory enzyme of gluconeogenesis that catalyzes the hydrolysis of fructose-1,6-bisphosphate to generate fructose-6-phosphate and inorganic phosphate. Deficiency of fructose-1,6-bisphosphatase is associated with fasting hypoglycemia and metabolic acidosis because of impaired gluconeogenesis. We have cloned and characterized the human liver fructose-1,6-bisphosphatase gene (FBP1). FBP1, localized to chromosome bands 9q22.2-q22.3 by fluorescence in situ hybridization, consists of seven exons that span > 31 kb, and the six introns are in the same position as in the rat gene. FBP1 was screened for mutations in two subjects with fructose-1,6-bisphosphatase deficiency. Four nucleotide substitutions were identified, two of which were silent mutations in the codons for Ala-216 (GCT-->GCC) and Gly-319 (GGG-->GGA). The other substitutions were in intron 3, a C-->T substitution 7 nucleotides downstream from the splice donor site, and in the promoter region, an A-->T substitution 188 nucleotides upstream from the start of transcription. These nucleotide substitutions were also found in normal unaffected subjects and thus are not the cause of fructose-1,6-bisphosphatase deficiency in the two subjects studied. The molecular basis of hepatic fructose-1,6-bisphosphatase deficiency in these subjects remains undetermined but could result from unidentified mutations in the promoter that decrease expression or from mutations in another gene that indirectly lead to decreased fructose-1,6-bisphosphatase activity.

Amino Acid Sequence↗
PubMed1995

Diabetes-like renal glomerular disease in Fanconi-Bickel syndrome.

The Fanconi-Bickel syndrome is a rare inherited disorder of metabolism characterized by hepatic glyconeogenesis, galactose intolerance, renal Fanconi syndrome with nephromegaly, and glycogen accumulation in proximal renal tubular cells. An 8-year-old patient with this disease and severe rickets due to medically resistant hypophosphatemia was found to have the previously unrecognized complication of renal glomerular hyperfiltration, microalbuminuria, and diffuse glomerular mesangial expansion. Similar to patients with glucose-6-phosphatase deficiency, the glomerular disease in this patient resembles incipient diabetic nephropathy. The Fanconi syndrome may be due to the defective transport of glucose at the proximal tubular basolateral membrane, which results in accumulation of glucose and secondarily glycogen within tubular cells. Since the metabolic defect, as evidenced by glycogen accumulation, selectively involves proximal renal tubular cells in the kidney of patients with Fanconi-Bickel syndrome and glucose-6-phosphatase deficiency, the abnormalities in renal glomerular hemodynamics and mesangial construct in these rare diseases are likely due to renal tubular factors, if the mechanism originates in the kidney. A delineation of these phenomena may further our understanding of the pathogenesis of diabetic nephropathy.

Albuminuria↗
PubMed1995

"Is this man your daddy?" suggestibility in children's eyewitness identification of a family member.

Studies of natural language development suggest that overextension of family memberships terms, such as daddy or papa, occurs in children in the second year of life, but rarely persists thereafter. However, in British Courts it is common for the testimony of 3- and even 4-year-olds to be dismissed on the grounds that these children may not be reliably identifying their father or stepfather when they claim that daddy was the perpetrator of abuse. This study examined whether 3-year-olds could be persuaded to confirm that a stranger who was labelled as daddy was their own father. A mock interview with experienced disclosure interviewers was conducted. Five of the 17 children--all from blue-collar families--misidentified a photograph of their own father when an identification question was repeated. Rather than undermining the validity of all preschoolers testimony, it is suggested that the responses of some children to apparently mundane questions of fact are influenced by contextual factors, including repetition of the question and the perceived omniscience of the interviewer.

Child Abuse↗
PubMed1995

Twin-twin transfusion syndrome: intraamniotic pressure measurement in the assessment of volume reduction at serial amniocenteses.

Two cases of severe twin-twin transfusion syndrome are described. In both, serial amniocenteses were followed by resolution of the disordered inter-twin haemodynamics with 4 intact term survivors. In all reports to date of aggressive reduction with or without successful outcome, volume reduction has been dictated by subjective or semiquantitative ultrasonic estimates of liquor volume. With the use of intraamniotic pressure estimation we describe a more rational basis for the removal of these large volumes of amniotic fluid.

Acute Disease↗
PubMed1995

Carotid steal syndrome: a case study.

The progression of subclavian arterial stenosis and the subsequent formation of collateral pathways serve to alter the pressure gradients in subclavian steal syndrome, altering ipsilateral vertebral artery flow from its normal state to "latent," "transient," and "continuous" steals. A similar altered flow in the carotid arteries can be observed with stenosis of the proximal common or innominate artery. A 59-year-old man was seen in the vascular laboratory for evaluation of symptomatic peripheral arterial disease. An incidental asymptomatic stenosis of the right innominate and left proximal subclavian artery was found. Further cerebral vascular evaluation displayed a continuous right subclavian steal and a latent steal in the right internal carotid artery. Transcranial Doppler examination displayed "transient" steal in the terminal right internal carotid artery. Combining duplex and transcranial Doppler evaluations allows sequential evaluation of the progression of arterial disease and its effect on the flow patterns in the cerebral vasculature.

Blood Flow Velocity↗
PubMed1995

Impaired glucose tolerance and increased weight gain in transgenic rats overexpressing a non-insulin-responsive phosphoenolpyruvate carboxykinase gene.

The effects of an overexpressed, non-insulin-responsive gluconeogenic enzyme, phosphoenolpyruvate carboxykinase (GTP) (PEPCK; EC 4.1.1.32), on glucose homeostasis were investigated. Transgenic rats harboring a metallothionein-driven PEPCK gene (lacking the entire PEPCK upstream-regulatory region) expressed transgene PEPCK mRNA in the key gluconeogenic tissues, liver and kidney. Female transgenic rats, studied at 10 weeks of age, showed mild fasting hyperglycemia (6.9 +/- 0.2 vs. 5.9 +/- 0.1 mM P = 0.002 n = 6), hyperinsulinemia (92.2 +/- 4.0 vs. 54.0 +/- 6.6 pM, P = 0.001, n = 6), impaired glucose tolerance and increased weight gain (178.3 +/- 3.2 vs. 153.4 +/- 2.5 g, P = 0.001, n = 16 and n = 13 transgenic and control rats, respectively). Despite hyperinsulinemia at this age, kidneys of transgenic rats maintained a significant 20% elevation of total PEPCK enzyme activity, while total liver PEPCK activity was not reduced. This study suggests that an insulin-resistant step in the gluconeogenic pathway can lead to glucose intolerance and an increase in weight. These rats offer the unique opportunity to study the metabolic consequences of chronic, mild excess glucose supply, as seen in non-insulin-dependent diabetes.

Animals↗
PubMed1995

Physician-patient communication in managed care.

The quality of physician-patient communication affects important health care outcomes. Managed care presents a number of challenges to physician-patient communication, including shorter visits, decreased continuity, and lower levels of trust. Good communication skills can help physicians create and maintain healthy relationships with patients in the face of these challenges. We describe 5 communication dilemmas that are common in managed care and review possible solutions suggested by recent literature on physician-patient communication. We also describe ways that managed care plans can promote more effective communication between physicians and patients.

Communication↗
PubMed1995

Phase I clinical trial of pyrazoloacridine NSC366140 (PD115934).

The pyrazoloacridine (PZA) analogue NSC366140 (PD115934) entered clinical trial based on unique preclinical characteristics including solid tumor selectivity in vitro, marked antitumor activity in vivo against murine solid tumors, selectivity against noncycling cells, and activity against multidrug-resistant tumor cells. After identification of the pre-clinical efficacy and an acceptable toxicity profile, a Phase I study of PZA was carried out. A total of 28 patients was entered and received a total of 67 treatment courses. The drug was administered via a 1-h infusion every 21 days. The starting dose was 30 mg/m2 with 2-fold dose escalations through 480 mg/m2. The next dose escalation was 50%, to 720 mg/m2. Grade I through grade IV toxicities were observed. Since no dose-limiting toxicities were observed at 480 mg/m2, and up to grade IV toxicities were observed at 720 mg/m2, an intermediate dose, 600 mg/m2, was evaluated. Dose-limiting toxicities at 720 mg/m2 were hematological (grade III and IV neutropenia) in four of six patients and neurological (up to grade III cerebral toxicities, including restlessness, dizziness, agitation/anxiety, personality changes, and nightmares, as well as myoclonus) in three of six patients treated. The pharmacokinetic parameters which helped predict these toxicities included area under the curve and peak plasma level. Pharmacokinetic studies showed interpatient variations in all parameters studied. The mean area under the curve levels of PZA at the highest two dose levels in patients were near the level detected in mice at their maximum tolerated total dose. The recommended starting dose for Phase II trials using this schedule is 600 mg/m2.

Acridines↗
PubMed1994

Glycogen storage disease in adults.

OBJECTIVE: To identify complications amenable to prevention in adults with glycogen storage disease (GSD) types Ia, Ib, and III and to determine the effect of the disease on social factors. DESIGN: Case series and clinical review. SETTING: Referral medical centers in the United States and Canada. PATIENTS: All patients with GSD-Ia (37 patients), GSD-Ib (5 patients), and GSD-III (9 patients) who were 18 years of age or older. MEASUREMENTS: Ultrasound or radiographic studies identified liver adenomas, nephrocalcinosis, or kidney stones. Radiographic studies identified osteopenia. Reports of the clinical examination, serum chemistry results, and social data were obtained. RESULTS: For patients with GSD-Ia, problems included short stature (90%), hepatomegaly (100%), hepatic adenomas (75%), anemia (81%), proteinuria or microalbuminuria (67%), kidney calcifications (65%), osteopenia or fractures or both (27%), increased alkaline phosphatase (61%) and gamma-glutamyltransferase (93%) activities, and increased serum cholesterol (76%) and triglyceride (100%) levels. Hyperuricemia was frequent (89%). Patients with GSD-Ib had severe recurrent bacterial infections and gingivitis. In patients with GSD-III, 67% (6 of 9) had increased creatinine kinase activity. Four of these patients had myopathy and cardiomyopathy. CONCLUSIONS: For GSD-Ia, hyperuricemia and pyelonephritis should be treated to prevent nephrocalcinosis and additional renal damage. For GSD-Ib, granulocyte-colony-stimulating factor may prevent bacterial infections. For GSD-III, more data are required to determine whether the myopathy and cardiomyopathy can be prevented. Most of the patients with GSD-I and GSD-III had 12 or more years of education and were either currently in school or employed.

Adult↗
PubMed1994

Extracellular ATP induces stellation and increases glial fibrillary acidic protein content and DNA synthesis in primary astrocyte cultures.

A number of factors appear to be involved in the proliferative and hypertrophic processes which characterize reactive astrocytosis. We have investigated the possibility that ATP, an agent that is released by injured cells following tissue destruction, may be one such factor. For this purpose, we utilized primary cultures of astrocytes derived from cerebral cortices of neonatal rats to study the effect of extracellular ATP on properties associated with astrogliosis. Light microscopic studies disclosed marked stellation of astrocytes after 30-60 min of exposure to 100 microM-1 mM ATP. In addition, the content of the astrocyte-specific intermediate filament, glial fibrillary acidic protein (GFAP), was increased 35-40% following 60-min exposure to ATP; this effect persisted for 1-3 days of exposure to 100 microM ATP. [3H]Thymidine incorporation increased progressively from 1-3 days; a 3.6-fold increase in DNA synthesis was observed following 3 days of exposure to 1 mM ATP, suggesting stimulation of cellular proliferation. These findings show that high micromolar to low millimolar concentrations of extracellular ATP reproduce several features associated with reactive gliosis and suggest that extracellular ATP may be involved in the activation of astrocytes following CNS injury.

Adenosine Triphosphate↗
PubMed1994

Response rates--an evolution.

The documented frequency of response of cancers to common chemotherapy agents and combinations appears to have decreased over the decades. Multiple reasons exist for this decline including: changes in eligibility and evaluability criteria; changes in the type of patients entered onto trial; and, altered criteria for response and methods for response assessment. The disinclination to publish negative results also permits a bias in a favor of overestimating a drug's efficacy. Circumspection now is advised in assessing data from older trials.

Antineoplastic Agents↗
PubMed1994

Randomized clinical trial of mitomycin-C with or without pretreatment with WR-2721 in patients with advanced colorectal cancer.

The use of mitomycin for metastatic colorectal cancer has been limited by mitomycin's myelosuppressive potential. The objective of this randomized study was to determine whether WR-2721 would decrease the hematologic toxicity of mitomycin in patients with colorectal cancer resistant to fluorouracil-based therapy. Ninety-seven patients with refractory colorectal cancer were randomized to receive either mitomycin 20 mg/m2 only or the same dose of mitomycin after pretreatment with WR-2721, 910 mg/m2. The principal toxicity in both groups was thrombocytopenia. The platelet nadirs were lower in patients receiving single-agent mitomycin (P = 0.026). Surprisingly, no clinical complete or partial responses were noted in either group, and survival was not different between the two groups. Thus, while WR-2721 decreased the thrombocytopenia associated with mitomycin therapy, mitomycin was ineffective in the treatment of refractory colorectal carcinoma.

Adult↗