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Biomedical subjects

M D Walker

Publications and source records attributed to M D Walker.

At least 19 recordsLinked to original sources
PubMed2006

Determinants of bone mineral density in Chinese-American women.

SUMMARY: Few data are available regarding bone mineral density (BMD) and its determinants among Chinese Americans. We identified determinants of BMD among 359 Chinese-American women in order to identify risk factors for low BMD in this burgeoning population. BMD in Chinese-American women is influenced by a number of factors, including immigration. INTRODUCTION: Osteoporosis and low BMD are common among Chinese women, including Chinese Americans, who are a growing population at risk for osteoporosis in the US. Few data are available regarding BMD and its determinants among Chinese-American women. METHODS: In this study, we examined predictors of BMD in 359 ambulatory Chinese-American women, ages 20-90, using stepwise multiple regression analysis. Variables in the model included age, weight, height, menarche age, years since menopause, immigration age, years in US, percentage of life in US, number of pregnancies, oral contraceptive use, family history of osteoporosis, family history of hip fracture, daily calcium intake, exercise, time outdoors, alcohol consumption and tobacco use. RESULTS: Among premenopausal women, weight was the strongest predictor of BMD, accounting for 10.5% of the variance at the lumbar spine (LS), 15.2% at the total hip (TH) and 16.6% at the femoral neck (FN). Time outdoors was also a positive predictor of BMD (1.4% at LS, 2.8% at TH and 1.6% at FN), while family history of osteoporosis (1.4% at TH) and age (3.7% at FN) were negative predictors. Among postmenopausal women, greater BMD at the LS and TH was associated with greater weight and earlier immigration age. Weight accounted for 16.4% of the variance at the LS and 19.8% at the TH; immigration age accounted for 3.1% of the variance at the LS and 4.1% at the TH. At the FN, years since menopause and weight were predictors of BMD, accounting for 14.4% and 8.7% of the variance, respectively. While older age at immigration had a negative effect on BMD, years in and proportion of life in the United States were not significant predictors of BMD. CONCLUSIONS: Bone mineral density in Chinese-American women is influenced by a number of biological and lifestyle factors, including immigration. The results of this study provide new insights into risk factors for low bone density as they relate to environmental determinants in the growing population of Chinese-American women.

Adult↗
PubMed2005

Neuroparasitic infections: nematodes.

Globalization has produced an increase in the number of people at risk for contracting parasitic infection. Central nervous system infection by nematodal parasites can be devastating. Early recognition and treatment of infection can significantly decrease morbidity of the parasitic infection, as well as the risk of secondary superinfection. The clinical presentation, diagnosis, and treatment for five of the more common nematodal infections of the nervous system--Angiostrongylus spp., Baylisacaris procyonis, Gnathostoma spinigerum, Strongyloides stercoralis, and Toxocara spp.--is reviewed.

Angiostrongylus↗
PubMed2005

Neuroparasitic infections: cestodes, trematodes, and protozoans.

Parasitic infection of the nervous system can produce a variety of symptoms and signs. Because symptoms of infection are often mild or nonspecific, diagnosis can be difficult. Familiarity with basic epidemiological characteristics and distinguishing radiographic findings can increase the likelihood of detection and proper treatment of parasitic infection of the nervous system. This article discusses the clinical presentation, diagnosis, and treatment for some of the more common infections of the nervous system caused by cestodes, trematodes and protozoans: Echinococcus spp., Spirometra spp. (sparganosis), Paragonimus spp., Schistosoma spp., Trypanosoma spp., Naegleria fowlerii, Acanthamoeba histolytica, and Balamuthia mandrillaris.

Animals↗
PubMed2001

Therapeutic ultrasound and wound closure: lack of healing effect on x-ray irradiated wounds in murine skin.

OBJECTIVE: To evaluate the efficacy of ultrasonography as a therapeutic agent in wound healing. DESIGN: Randomized, controlled trial. SETTING: University animal laboratory. ANIMALS: Male BALB/c mice randomly allocated to 5 groups. INTERVENTIONS: In group 1, mice were left untreated; in groups 2 through 5, a well-defined area on the dorsum was exposed to 20Gy x-ray irradiation. Seventy-two hours postirradiation, all mice were anesthetized by inhalation (isoflurane anesthetic) and a 7 x 7mm area wound made on the dorsum. All wounds were videotaped alongside a marker scale 3 times weekly until closure was complete. Mice in groups 4 and 5 were treated with pulsed therapeutic ultrasound for 5 minutes, 3 times weekly at 1 and 3MHz, respectively (intensity, 0.5W/cm(2)); mice in group 3 received placebo ultrasound. Subsequently, the area of each wound was measured from video by using an image analysis system. MAIN OUTCOME MEASURE: Wound closure as a fraction of day zero. RESULTS: Irradiation caused a significant (p < .01) delay in the rate of wound closure by day 11. However, neither placebo ultrasound nor treatment at 1 or 3MHz affected the closure rate. CONCLUSION: These findings provide little evidence that 1 or 3MHz ultrasound applied to a radiation-impaired wound stimulates wound closure in mice.

Analysis of Variance↗
PubMed2000

Recommendations for the establishment of primary stroke centers. Brain Attack Coalition.

OBJECTIVE: To develop recommendations for the establishment and operation of primary stroke centers as an approach to improve the medical care of patients with stroke. PARTICIPANTS: Members of the Brain Attack Coalition (BAC), a multidisciplinary group of representatives from major professional organizations involved with delivering stroke care. Supplemental input was obtained from other experts involved in acute stroke care. EVIDENCE: A review of literature published from 1966 to March 2000 was performed using MEDLINE. More than 600 English-language articles that had evidence from randomized clinical trials, meta-analyses, care guidelines, or other appropriate methods supporting specific care recommendations for patients with acute stroke that could be incorporated into a stroke center model were selected. CONSENSUS PROCESS: Articles were reviewed initially by 1 author (M.J.A.). Members of the BAC reviewed each recommendation in the context of current practice parameters, with special attention to improving the delivery of care to patients with acute stroke, cost-effectiveness, and logistical issues related to the establishment of primary stroke centers. Consensus was reached among all BAC participants before an element was added to the list of recommendations. CONCLUSIONS: Randomized clinical trials and observational studies suggest that several elements of a stroke center would improve patient care and outcomes. Key elements of primary stroke centers include acute stroke teams, stroke units, written care protocols, and an integrated emergency response system. Important support services include availability and interpretation of computed tomography scans 24 hours everyday and rapid laboratory testing. Administrative support, strong leadership, and continuing education are also important elements for stroke centers. Adoption of these recommendations may increase the use of appropriate diagnostic and therapeutic modalities and reduce peristroke complications. The establishment of primary stroke centers has the potential to improve the care of patients with stroke. JAMA. 2000.

Clinical Protocols↗
PubMed2000

Transcription factor BETA2 acts cooperatively with E2A and PDX1 to activate the insulin gene promoter.

The insulin gene is efficiently expressed only in pancreatic beta cells. Using reverse transcriptase-polymerase chain reaction analysis, we show that insulin mRNA levels are at least 10(5)-fold higher in beta cells than non-beta cells. To examine the underlying mechanisms, we expressed beta cell transcription factors by transfection of non-beta cells. Separate expression of BETA2, E2A, or PDX1 led to modest (<10-fold) activation of the insulin promoter, whereas co-expression of the three proteins produced synergistic, high level activation (160-fold). This level of activity is approximately 25% that observed in transfected beta cell lines. Of the three factors studied, BETA2 appears to play a dominant role. Efficient transcription required a C-terminal activation domain of BETA2 and an N-terminal region, which does not function as an independent activation domain. The myogenic basic helix-loop-helix (bHLH) protein MyoD was unable to bind and activate the promoter, even when its DNA binding region was replaced with that of BETA2. Our results demonstrate the central importance of BETA2 in insulin gene transcription and the importance of sequences outside the canonical DNA binding domain in permitting efficient DNA binding and cell-specific activity of the insulin gene promoter.

Animals↗
PubMed2000

Effect of low-intensity laser irradiation (660 nm) on a radiation-impaired wound-healing model in murine skin.

BACKGROUND AND OBJECTIVE: The use of low-intensity laser therapy (LILT) as a therapeutic modality has become popular in a variety of clinical applications including the promotion of wound repair. Although the clinical evidence base for such application remains sparse, recent studies have demonstrated a number of quantifiable photobiological effects associated with such therapy. In the present study, the effect of laser irradiation at various radiant exposures on a radiation-impaired wound-healing model in murine skin was investigated. STUDY DESIGN/MATERIALS AND METHODS: The study included two phases; in phase one, male Balb/c mice (n = 36; age-matched at 10 weeks) were randomly allocated to three experimental groups (n = 12, each group). In all groups, a well-defined area on the dorsum was exposed to 20 Gy x-rays. Seventy-two hours postirradiation, all mice were anaesthetised and a 7 x 7 mm area wound was made on the dorsum. All wounds were videotaped alongside a marker scale (three times weekly) until closure was complete. In groups 2 and 3, mice were treated with laser irradiation (0.5 and 1.5 J/cm(2), respectively) three times weekly by using a 660-nm GaAlAs laser unit (5 kHz; 15 mW; Omega Laser Systems, London, UK). Wound areas were then calculated by using an image analysis system (Fenestra 2.1), and results were analyzed by using repeated measures and one-factor analysis of variance statistical tests. In phase two, two experimental groups were included (n = 12 each group); the protocol was identical to that described for phase 1; however, mice in group 2 were treated with a radiant exposure of 4 J/cm(2). RESULTS: Results from this investigation demonstrated that treatment with 0.5, 1.5. and 4 J/cm(2) had no beneficial effect on the rate of wound closure (P > 0.05). CONCLUSION: These findings provide little evidence of the putative stimulatory effects of LILT in vivo at the parameters investigated.

Animals↗
PubMed1999

GRFbeta, a novel regulator of calcium signaling, is expressed in pancreatic beta cells and brain.

By screening for genes expressed differentially in pancreatic beta cells, we have isolated a cDNA encoding GRFbeta, a novel 178-amino acid protein whose N terminus is identical to that of GRF1, a calcium-dependent guanine nucleotide exchange factor, and whose C terminus is unrelated to known proteins. We show that both GRF1 and GRFbeta are expressed selectively in beta cell lines, pancreatic islet cells and brain. Treatment of beta cell lines (betaTC1 and HIT) with calcium ionophore led to a significant elevation in activity of the Ras signal transduction pathway, as determined by phosphorylation of extracellular signal-related kinase (ERK). Transfection of beta cells with a plasmid encoding a dominant negative variant of GRF1 led to 70% reduction in ERK phosphorylation, consistent with a role for GRF1 in calcium-dependent Ras signaling in these cells. To examine the possible function of GRFbeta, cultured cells were transfected with a GRFbeta expression vector. This led to a significant reduction in both GRF1-dependent ERK phosphorylation and AP1-dependent reporter gene activity. The results suggest that GRF1 plays a role in mediating calcium-dependent signal transduction in beta cells and that GRFbeta represents a novel dominant negative modulator of Ras signaling.

Amino Acid Sequence↗
PubMed1999

Nicotinamide-inhibited vasoconstriction: lack of dependence on agonist signalling pathways.

Previously, we have shown that nicotinamide inhibits both high [K+]- and phenylephrine-induced constrictions in a dose-dependent manner in rat tail arteries. We have now investigated the effect of nicotinamide on intracellular signalling pathways in vascular smooth muscle. Nicotinamide (8.2 mM) reduced the response to phenylephrine- and [Arg8]vasopressin-induced constrictions by means of 72.9+/-6.9 and 51.8+/-5.7%, respectively. It also blocked phenylephrine-induced constrictions in the absence of a functional endothelium (P < 0.0136). In addition, pre-treatment of the artery with nifedipine (10 mM) also failed to inhibit nicotinamide's activity (P < 0.0178). Moreover, nicotinamide significantly reduced the sensitivity to phenylephrine in Ca2+-free Krebs' solution (P < 0.0152). Continuous perfusion of maximal concentrations of ryanodine or thapsigargin significantly inhibited the response to phenylephrine; the addition of nicotinamide (8.2 mM) caused a significant additional inhibition when compared to the effect of ryanodine (P < 0.0006) or thapsigargin (P<0.037) alone. In addition, beta-escin (0.02%) permeabilisation and Ca2+ (2.5 mM)-mediated constriction was also significantly attenuated by nicotinamide (P < 0.0001). However, phorbol ester-induced constriction was not attenuated by nicotinamide. This would suggest that nicotinamide directly inhibits vascular smooth muscle cell contraction and is unlikely to act via blockage of external Ca2+ entry or release of Ca2+ from intracellular stores.

Animals↗
PubMed1999

Specific gene expression in pancreatic beta-cells: cloning and characterization of differentially expressed genes.

Identification and characterization of genes expressed preferentially in pancreatic beta-cells will clarify the mechanisms involved in the specialized properties of these cells, as well as providing new markers of the development of type 1 diabetes. Despite major efforts, relatively few beta-cell-specific genes have been characterized. We applied representational difference analysis to identify genes expressed selectively in the pancreatic beta-cell line betaTC1 compared with the pancreatic alpha-cell line alphaTC1 and isolated 26 clones expressed at higher levels in the beta-cells than in the alpha-cells. DNA sequencing revealed that 14 corresponded to known genes (that is, present in GenBank). Only four of those genes had been shown previously to be expressed at higher levels in beta-cells (insulin, islet amyloid polypeptide, neuronatin, and protein kinase A regulatory subunit [RIalpha]). The known genes include transcription factors (STAT6) and mediators of signal transduction (guanylate cyclase). The remaining 12 genes are absent from the GenBank database or are present as expressed sequence tag (EST) sequences (4 clones). Some of the genes are expressed in a highly specific pattern-expression in betaTC1 and islet cells and in relatively few of the non-beta-cell types examined; others are expressed in most cell types tested. The identification of these differentially expressed genes may aid in attaining a clearer understanding of the mechanisms involved in beta-cell function and of the possible immunogens involved in development of type 1 diabetes.

Amyloid↗
PubMed1998

Differential expression of the protein kinase A regulatory subunit (RIalpha) in pancreatic endocrine cells.

A PCR-based subtractive cloning procedure was used to identify genes expressed at higher levels in the pancreatic beta cell line betaTC1, as compared to the pancreatic alpha cell line alphaTC1. One of the clones isolated by this procedure corresponded to the regulatory subunit (RIalpha) of protein kinase A (PKA). Using antibodies directed against RIalpha, we now demonstrate both by immunoblot and immunofluorescence that RIalpha protein is present at higher levels in cultured beta cells as compared to alpha cells. In vitro PKA assays revealed high basal PKA activity in alphaTC1 extracts, which changed little on addition of exogenous cAMP. On the other hand, extracts from beta cells showed very low basal activity of PKA, which was elevated upon addition of cAMP. A similar trend was observed in vivo using transfected luciferase constructs bearing multiple copies of a CRE element: in alphaTC1 cells, no induction by forskolin was observed, whereas in betaTC1 cells, forskolin produced a 9-fold increase in activity. Therefore, the results indicate that RIalpha of PKA is selectively expressed in pancreatic beta cells as compared to alpha cells: this selective expression is associated with major differences in the properties of the PKA signal transduction pathway. Differential expression of the regulatory subunit may play a role in determining the patterns of gene expression and signal transduction characteristic of alpha and beta cells.

Cell Line↗
PubMed1998

Effect of low intensity monochromatic light therapy (890 nm) on a radiation-impaired, wound-healing model in murine skin.

BACKGROUND AND OBJECTIVE: The use of low intensity laser and monochromatic light diodes as a therapeutic modality has become popular in a variety of clinical applications, including the promotion of wound repair. Despite this, the clinical evidence base for such application remains sparse; in contrast, recent studies have demonstrated a number of quantifiable photobiological effects associated with such therapy. In the present study, the effect of low intensity monochromatic light irradiation (MLI) at various radiant exposures upon a radiation-impaired wound model in murine skin was investigated. STUDY DESIGN/MATERIALS AND METHODS: Male Balb/c mice (n = 50; age matched at 10 weeks) were randomly allocated to five experimental groups (n = 10 each group). In Group 1, mice were left untreated; in Groups 2-5, a well-defined area on the dorsum was exposed to 20 Gy X-ray irradiation. At 72 hours postirradiation, all mice were anaesthetised and a 7-mm-square area wound was made on the dorsum. All wounds were videotaped alongside a marker scale until closure was complete. In Groups 3-5, mice were treated with MLI (0.18, 0.54, and 1.45 J/cm2, respectively) three times weekly using a GaAlAs 890 nm multidiode (n = 60) array unit (270 Hz; maximum rated output, 300 mW; Anodyne, Denver, CO). Subsequently, the area of each wound was measured from video using an image analysis system (Fenestra 2.1), and results were analysed using repeated measure and one-factor ANOVA statistical tests. RESULTS: X-ray irradiation caused a significant delay (P = 0.0122) in healing by day 7. MLI at 0.18 J/cm2 and 0.54 J/cm2 had no effect upon the rate of wound closure. However, a highly significant (P = 0.0001) inhibition occurred following MLI irradiation at 1.45 J/cm2 by day 16. CONCLUSION: These findings provide little evidence of the putative stimulatory effects of monochromatic light irradiation in vivo, but, rather, reveal the potential for an inhibitory effect at higher radiant exposures.

Analysis of Variance↗
PubMed1998

The differentiation of Phytophthora species that are pathogenic on potatoes by an asymmetric PCR combined with single-strand conformation polymorphism analysis.

The goal of this study was to develop a polymerase chain reaction (PCR) capable of differentiating Phytophthora species that are pathogenic on potatoes using a single primer pair. To achieve this objective, primers were derived from conserved regions flanking variable sequences in the internal transcribed spacer 1 (ITS1) of Phytophthora species. One primer pair produced a 140 bp product from P. infestans, P. erythroseptica and P. nicotianae. The PCR products were purified and used in an asymmetric PCR (A-PCR) protocol to generate single-strand DNA (ssDNA). The ssDNA of the Phytophthora potato pathogens reproducibly migrated in non-denaturing polyacrylamide gels in a species-specific manner.

Base Sequence↗
PubMed1998

Cost-effectiveness of tissue plasminogen activator for acute ischemic stroke. NINDS rt-PA Stroke Study Group.

Tissue plasminogen activator (tPA) has been shown to improve 3-month outcome in stroke patients treated within 3 hours of symptom onset. The costs associated with this new treatment will be a factor in determining the extent of its utilization. Data from the NINDS rt-PA Stroke Trial and the medical literature were used to estimate the health and economic outcomes associated with using tPA in acute stroke patients. A Markov model was developed to estimate the costs per 1,000 patients eligible for treatment with tPA compared with the costs per 1,000 untreated patients. One-way and multiway sensitivity analyses (using Monte Carlo simulation) were performed to estimate the overall uncertainty of the model results. In the NINDS rt-PA Stroke Trial, the average length of stay was significantly shorter in tPA-treated patients than in placebo-treated patients (10.9 versus 12.4 days; p = 0.02) and more tPA patients were discharged to home than to inpatient rehabilitation or a nursing home (48% versus 36%; p = 0.002). The Markov model estimated an increase in hospitalization costs of $1.7 million and a decrease in rehabilitation costs of $1.4 million and nursing home cost of $4.8 million per 1,000 eligible treated patients for a health care system that includes acute through long-term care facilities. Multiway sensitivity analysis revealed a greater than 90% probability of cost savings. The estimated impact on long-term health outcomes was 564 (3 to 850) quality-adjusted life-years saved over 30 years of the model per 1,000 patients. Treating acute ischemic stroke patients with tPA within 3 hours of symptom onset improves functional outcome at 3 months and is likely to result in a net cost savings to the health care system.

Acute Disease↗
PubMed1998

A review of quality of life in Alzheimer's disease. Part 1: Issues in assessing disease impact.

There are numerous methods available for assessing patients with Alzheimer's disease (AD) or other forms of dementia. Quality-of-life (QOL) assessment is unique among these methods, because the QOL concept itself includes a subjective component that is fundamental to its measurement. It could be argued that measuring quality of life is just as important as measuring disease severity, disease progression, symptom response, cognition, behavioural disturbance and activities of daily living when assessing the impact of disease and intervention in dementia. The subjective nature of quality of life provides healthcare professionals with the opportunity of incorporating the value systems of patients and their carers into their assessments. A systematic review was carried out to include the published data (and some unpublished data) on QOL assessment tools and instruments that claim to measure quality of life in dementia. Literature for this review was identified by a thorough search of computer databases (1980-1997) that included Medline, Embase, PsychLit and International Pharmaceutical Abstracts. Reports concerning the conceptualisation, development, validation, reliability, reproducibility, comprehensiveness, practicality and use of QOL instruments in dementia/AD were selected for review as well as papers documenting clinical drug trials in this therapeutic area. A number of measures or methods used in the literature for assessing the quality of life of patients with dementing illnesses were identified. It was decided to present the resulting review in 2 parts that correspond to the 2 main groups into which the instruments were categorised. The first (part 1) looks at measures used to assess the impact of disease as well as instruments at a developmental or testing stage. The second (part 2) includes instruments that claim to measure quality of life in studies documenting the impact of a drug in this therapeutic area. There are as yet no validated methods of assessing the quality of life of both patients with dementia and their carers at the same time. QOL outcomes for these 2 groups is closely, if not fundamentally, linked and yet most studies identified in this review concentrate on measuring the quality of life of either the patient or the carer alone. Although some researchers may be getting close conceptually, an instrument has yet to satisfy all the criteria necessary to become accepted as a gold standard for QOL assessment in dementing illness. The ideal instrument must show that it can reliably, reproducibly and comprehensively assess quality of life for patients with dementia and their carers. It should also demonstrate that it can measure quality of life effectively using a practical administration technique that does not place any unnecessary burden on either informal carers, other healthcare workers involved or the patient themselves. Further cross-sectional and longitudinal research is required to psychometrically test the available instruments as well as continuing conceptual research to explore new ways of assessing quality of life in this important area.

Aged↗
PubMed1998

A review of quality of life in Alzheimer's disease. Part 2: Issues in assessing drug effects.

There are numerous methods available for assessing patients with Alzheimer's disease (AD) or other forms of dementia. Quality-of-life (QOL) assessment is unique among these methods. The subjective nature of quality of life provides healthcare professionals with the opportunity of incorporating the value systems of patients and their carers into their assessments. A systematic review was carried out to assess the published data (and some unpublished data) on QOL assessment tools and instruments that claim to measure quality of life in dementia. A number of measures or methods used in the literature for assessing the quality of life of patients with dementing illnesses were identified. It was decided to present the resultant review in 2 parts that correspond to the 2 main groups into which the instruments were categorised. The first (part 1), looked at measures used to assess the impact of disease as well as instruments at a developmental or testing stage. The second (part 2), includes instruments that claim to measure quality of life in studies documenting the impact of a drug in this therapeutic area. This second group consists mainly of instruments identified as being used to assess quality of life during clinical trials in dementia/AD. As in part 1, this part of the review was unable to identify any validated methods of assessing the quality of life of both patients with dementia and their carers at the same time. The ideal instrument must show that it can reliably, reproducibly and comprehensively assess quality of life for both patients with dementia and their carers. It should also demonstrate that it can measure quality of life effectively using a practical administration technique that does not place any unnecessary burden on either informal carers, other healthcare workers involved or the patient themselves. In addition, any measure intended for use in assessing the impact of drug treatment on quality of life must demonstrate sensitivity to change, also known as responsiveness. All these criteria are even more important when measuring quality of life as an outcome during clinical trials of a new antidementia drug, because the data generated are likely to influence decisions made by regulatory bodies about whether to grant licences that are required by pharmaceutical companies to market their products. Further cross-sectional and longitudinal research is required to ensure that the available instruments possess the essential psychometric criteria that must be demonstrated prior to their utilisation in clinical trials of any compound developed for use in dementia/AD. Ongoing conceptual research may still be useful in exploring new ways of assessing quality of life in this important therapeutic area.

Alzheimer Disease↗
PubMed1997

Functional characterization of the trout insulin promoter: implications for fish as a favorable model of pancreas development.

The complex anatomy of the mammalian pancreas, in which the endocrine cells are grouped in islets dispersed among the predominant exocrine component, has hampered study of the molecular events governing the development of pancreatic cell lineages. To investigate whether fish may provide relevant, complementary models of pancreas development, we characterized the trout insulin (tINS) promoter and its molecular interactions with PDX1, a key transcriptional and developmental factor of the mammalian pancreas. Transfection of a luciferase reporter plasmid containing the 280 bp 5'-flanking region of the tINS gene resulted in strong activity in mammalian pancreatic beta cells but not in CHO or pituitary cells. Footprinting assays and cotransfection experiments indicated that mammalian PDX1 binds to and activates the tINS promoter. By microinjecting plasmids to fertilized zebrafish eggs, we showed that the expression of mouse PDX1 is capable of activating the co-injected tINS promoter plasmid in most cell types of the 24-h zebrafish embryo. The conserved role of PDX1 in vertebrate insulin gene regulation opens the possibility to exploit fish models in the study of pancreas development.

Animals↗