[Modified Risdon approach for the treatment of subcondylar fractures of the mandible].
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Adolescent↗
Biomedical subjects
S Zink
Publications and source records attributed to S Zink.
Systematic assessment of atypical deletions reveals genotype-phenotype correlation in 22q11.2.
INTRODUCTION: Clinical variability associated with the common 22q11.2 microdeletion is well known, and has led to a broad application of FISH diagnostics with probes for loci TUPLE1 or D22S75 (N25), although, rarely reported atypical deletions associated with the same phenotypic spectrum would not be discovered by these probes. As most types of 22q11.2 deletions occur between low copy repeats within the region (LCR22), we assumed that atypical deletions should be more common than has been reported. To address this question and the possibility of a deletion size related genotype-phenotype correlation, we systematically assessed the frequency of typical and atypical 22q11.2 deletions in a large cohort of patients. METHODS: We used a set of 10 fluorescent in situ hybridisation (FISH) DNA probes, capable of detecting all reported and hypothetical deletions between the LCR22, and analysed 350 patients. Deletion sizes in atypical deletions were established by use of further FISH probes. Frequency of certain atypical deletions was analysed in controls by FISH and quantitative PCR. RESULTS: Patients with conotruncal heart defects (ctCHD) and with typical VCFS phenotype showed the common 3 Mb or nested 1.5 Mb deletions (in 18.5% and 78.6%, respectively), but no atypical deletion, while 5% (3/63) of patients with a mildly suggestive, atypical phenotype showed atypical distal deletions, which were not detected in patients with mental retardation of unknown origin or in healthy controls. DISCUSSION: These statistically significant differences demonstrate that atypical distal 22q11.2 deletions are very uncommon in patients with ctCHDs, while atypical congenital heart defects and mild dysmorphism are recognisable feature of atypical distal deletions. Further phenotype-genotype analysis disclosed association of significant developmental delay with the distal part of the common deletion region, and choanal atresia and atypical CHDs with the adjacent distal deletion region.
Chromosomes, Human, Pair 22↗
[Cervical origin of the subclavian artery: echocardiographic diagnosis in patients with monosomy 22q11].
OBJECTIVE: To assess the sensitivity and specificity of echocardiography in the detection of anomalies of the subclavian artery (cervical origin, aberrant origin from the descending aorta or isolation) in patients with monosomy 22q11. METHOD: From 1/1998 until 03/2002 we examined 57 patients with conotruncal cardiac malformations. 30 patients had pulmonary atresia and ventricular septal defect (53 %), 13 interrupted aortic arch (23 %), 9 tetralogy of Fallot (16 %) and 5 common truncus arteriosus (9 %). Echocardiographic examination included identification of the laterality of the aortic arch as well as examination of the origin of the brachiocephalic vessels. The results were compared with angiographic and intraoperative findings. Median age at echocardiographic investigation was 74 days (range 1 d - 33.4 yrs.). RESULTS: Laterality of the aortic arch was assessed correctly in all patients. 20/57 patients had a right-sided aortic arch (35 %). Echocardiography detected all anomalies of the subclavian artery (14/57 patients, 25 %, sensitivity 100 %) and excluded these anomalies correctly in 43 patients (specificity 100 %). Exact classification of the anomaly of the subclavian artery was possible in 6/6 patients with a cervical origin of the artery and in 7/8 patients with aberrant origin from the descending aorta. Monosomy 22q11 was diagnosed in 21 patients (37 %). CONCLUSION: Echocardiography achieves a high sensitivity in the detection of anomalies of the subclavian artery. The diagnosis of cervical origin of the artery, in particular, can be easily established. As this anomaly appears to be a specific marker for monosomy 22q11, echocardiography facilitates reliable identification of these patients in clinical practice.
Adolescent↗
Ascending arterial blood flow velocities during cardiac diastole in critical care patients--a characteristic flow pattern with a bad prognosis.
AIM: Pulsed Doppler ultrasound is a standard noninvasive investigation to measure the velocity and pulsatility of blood flow within the major intracranial and organ-supplying arteries in critical care patients. The normal arterial flow pattern in organ-supplying vessels is characterised by a systolic-diastolic forward flow which is caused by the aortic "Windkessel" function and the low peripheral resistance of the parenchymatous organs. A variety of well known pathological conditions may cause a change of the vascular characteristics within the perfused organs which are diagnosed by the typical changes of the flow pattern in the supplying arteries. In the cardiac diastole, however, there is always a slow decrease of the flow velocity which is terminated by the onset of the following systole. METHOD AND RESULTS: We report on 11 patients investigated by Doppler ultrasound during their stay in our intensive care unit. All these patients presented a markedly different flow pattern measured in their intra- and/or extracerebral vessels. This very distinctive flow pattern is characterised by a diastolic ascent of the arterial flow velocity and is caused by an excessively increased venous pressure within the draining veins of the affected organs. All patients died due to (multiple) organ failure. CONCLUSION: It is of major importance to be aware of the rare but very characteristic flow pattern described here because of the poor prognosis associated with it.
Arteries↗
Small pulmonary lesions--a challenge for thoracic surgery?
We analyzed the diagnosis, the potentially associated external and clinical features, and the surgical procedures of small pulmonary lesions, especially hamartomas (in relation to peripheral T1 lung carcinomas and lymphoid hyperplasia) in 103 patients who experienced enucleation or resection of pulmonary hamartomas between March 1, 1995 and December 31, 2000. The causes of surgical intervention, presurgical diagnoses, surgical procedures, location, size, and histological compartments were analyzed, as well as clinical features potentially associated with the tumors (alcohol, asbestos, smoking, and chronic lung diseases). Follow up of patients lasted for 5.5 years at maximum. For comparison, 36 patients with peripheral T1 lung carcinomas are included as well as 50 patients with lymphoid hyperplasia. The sex and age distribution of the patients with hamartomas was comparable to that of patients with lymphoid hyperplasia. About 75% of men and 55% of women were heavy smokers, with an average history of 30 and 17 pack years, respectively. In 84% of patients, the lesions were incidentally detected in chest radiographs, whereas 12% of patients underwent thoracic surgery suspicious for intrapulmonary metastases of known extrapulmonary malignancies. Enucleation was performed in 21%, and wedge resection in 77% of patients. At average, hamartomas were smaller than T1 lung carcinomas, but considerably larger in comparison to lymphoid hyperplasia. No recurrent tumors or additionally detected hamartomas were noted during the follow up, and both surgical procedures (enucleation or wedge resection) were identical in curative treatment. All patients with peripherally localized T1 tumors underwent lobectomy. The 3/5 year survival rate was calculated to 69/52%. Lymphoid hyperplasia is of clinical importance for the estimation of prognosis in patients with metastatic disease, as the number of radiologically suggestive metastatic nodules can often be significantly changed due to this entity. Pulmonary hamartomas are benign lesions that display certain clinical associations with malignant lung carcinomas in respect to external risk factors, and to lymphoid hyperplasia. Both surgical procedures (enucleation or wedge resection) can be performed, giving identical results in respect to treatment.
Adolescent↗
Glyco- and immunohistochemical refinement of the differential diagnosis between mesothelioma and metastatic carcinoma and survival analysis of patients.
The aim of this study was to analyse the diagnostic value of selected glyco- and immunohistochemical probes for discrimination between mesotheliomas and metastatic carcinomas within the pleura, and to evaluate prognostic indicators in the tested panel. A panel of nine markers (five antibodies, two neoglycoproteins, and labelled hyaluronic acid) was applied to a total of 264 specimens with mesotheliomas (118 cases) and metastatic carcinomas in the pleura (146 cases); the material consisted exclusively of surgical specimens. The diagnosis obtained by standard procedures was further substantiated through a detailed follow-up and clear-cut descriptions of primary sites. The metastatic tumours originated from the lung (82 cases), breast (47 cases), colon (three cases), and kidney (two cases); in 12 cases, however, the tumour origin could not be ascertained. In detail, the probes tested included antibodies against carcinoembryonic antigen (CEA), vimentin, calretinin, mesothelial cells (HBME-1), calcyclin and keratin-5; and also biotinylated neoglycoproteins with ganglioside GM1 and N-acetyl-D-glucosamine (GlcNAc) as the ligand part, and hyaluronic acid. Carrier-immobilized ganglioside GM1 and hyaluronic acid displayed the highest specificity and sensitivity for mesotheliomas, followed by calretinin and HBME-1, whereas keratin-5 and vimentin were of low specificity (43% and 52%, respectively). Metastatic carcinomas could be discerned by CEA detection and application of GlcNAc-bearing neoglycoprotein with similar sensitivity (76% and 72%, respectively) and specificity (91% and 86%, respectively). In cases of breast carcinoma, the maximum specificity (59%) and sensitivity (67%) were low for all markers. Patients with mesothelioma survived longer than those with metastatic carcinoma, especially those with detectable binding sites for hyaluronic acid. No association of tumour type and binding properties of the other applied probes with survival of the patients could be found at a statistically significant level. It is concluded that in routine practice, the application of carrier-immobilized GM1, hyaluronic acid, and antibodies against calretinin and HBME-1 is useful for confirmation of mesothelioma, whereas the detection of CEA and GlcNAc-specific binding sites is useful for distinguishing metastatic carcinoma from mesothelioma. Despite the rather infrequent occurrence of mesotheliomas in women, particular attention should be given to exclude or confirm metastatic breast carcinoma in cases of unknown history or long metastatic interval.
Acetylglucosamine↗
Endobronchial juvenile hemangioma--a case report of a neonate including immunohistochemical monitoring and nuclear, cellular, and vascular morphometry.
A 3-month-old female child suffered from tachypnea and dyspnea with abnormal blood gas values. Chest X-rays revealed an increased transparency of the left lung and a mediastinal shift to the right side. High resolution computed tomography (CT) documented a narrowing of the left upper stem bronchus. Ensuing endoscopy detected an occlusive endobronchial tumor mass that did not infiltrate the bronchial cartilage as confirmed with endobronchial ultrasonic monitoring. Based on gross histological examination of the surgical specimen obtained using sleeve resection, the highly vascularized tumor exhibited an adenomatoid growth pattern with a rather homogeneous population of nuclei. The light microscopical presentation was consistent with a juvenile (infantile) hemangioma, which was confirmed using immunohistochemical examinations despite the display of neuroendocrine features. Although endobronchial juvenile hemangiomas are an extremely rare event in early childhood, this case underscores the necessity to not neglect its occurrence in differential diagnosis.
Biomarkers, Tumor↗
Survival, disease-free interval, and associated tumor features in patients with colon/rectal carcinomas and their resected intra-pulmonary metastases.
OBJECTIVE: Colon/rectum cancer often presents with intrapulmonary metastases. Surgical resection can be performed in a selected group of patients. In this study, the search for possible prognostic factors of patients with primary colon/rectum cancer and lung metastases was performed. METHODS: Medical records of 110 patients operated on pulmonary metastases of primary colon/rectum cancer were reviewed. The clinical parameters include age, sex, pTNM/UICC stage, grading, localization, surgical and adjuvant therapy of the primary cancer. The number, maximum diameter and total intra-thoracic resected tumor-mass ('load'), the pre-thoracotomy serum carcinoembryonic antigen (CEA) levels, localization of the metastases (uni- vs. bilateral), the presence of hilar/mediastinal tumor-infiltrated lymph nodes, the surgical procedure and performed therapy schemes of lung metastases were recorded. RESULTS: The cumulated 5- and 10-year total survival after diagnosis of the primary carcinomas was estimated to 71 and 33.7%, respectively. After resection of the pulmonary metastases, the 3- and 5-year post-thoracotomy survival measured 57 and 32.6%, respectively. The median time interval between diagnosis of the primary cancer and thoracotomy (disease free interval (DFI)) was found to be 35 months. A non-negligible percentage of patients (15.4%) displayed limited tumor stages of the primary cancer (pT1/2, pN0). The median diameter of the largest metastasis measured 28 mm, and the median resected intrathoracic tumor-load was calculated to 11.4 cm(3). In only 8 patients hilar or mediastinal tumor-involved lymph nodes were found. A potentially curative resection of lung metastases was recorded in 96 patients. The overall survival was significantly correlated with the DFI and the number of intrapulmonary metastases. The DFI correlated significantly with the tumor load and the number of metastases; the post-thoracotomy survival with the number of metastases, tumor-load and pre-thoracotomy serum CEA level. Treatment, stage and grade of the primary cancer, occurrence of liver metastases and local recurrences, mode of treatment of metastases and postoperative residual stage had no significant correlation with either total nor post-thoracotomy survival. CONCLUSIONS: Pulmonary metastases occur even in patients with limited tumor-stages of primary colon/rectum cancer. DFI is the major parameter to estimate the total survival of patients with lung metastases. The survival after thoracotomy depends on the number of metastases, the intrapulmonary tumor load and the presence of elevated serum CEA level prior to thoracotomy.
Adult↗
The Rapid Syndrome Validation Project (RSVP).
The Rapid Syndrome Validation Project (RSVP) is a collaboration of several institutions: Sandia and Los Alamos National Laboratories, the University of New Mexico Department of Emergency Medicine, and the NM Department of Health Office of Epidemiology. RSVP is a system that operates at the intersection of individual health care providers, public health and bioterrorism. Physicians quickly enter clinical and demographic information on patients exhibiting symptoms and signs of the syndromes of interest. It provides early warning and response to emerging biological threats, as well as emerging epidemics and diseases. RSVP provides real time clinical information to the provider and any other potential user such as the DOH, about current symptoms, disease prevalence and location. The system also serves as a mechanism for the Department of Health to inform health care providers of health alerts and to facilitate the process of collecting data on reportable diseases. We describe here the purpose an the architecture of a network-based surveillance system that is currently implemented in an Emergency Department.
Bioterrorism↗
Benign metastasizing leiomyoma of the uterus: documentation of clinical, immunohistochemical and lectin-histochemical data of ten cases.
The clinical histories of 10 women suffering from benign metastasizing leiomyoma (BML) after hysterectomy and information on lung lesions detected in these women are presented, together with corresponding data for 2 women with metastasizing leiomyosarcoma of the uterus for comparison: gross appearance, survival, and light microscopical, immunohistochemical and lectin-histochemical findings are reported. All patients with BML had undergone hysterectomy for uterus leiomyomatosus without any detection of sarcomatous lesions in the uterus wall. After a median period of 14.9 years intrapulmonary masses were detected by imaging techniques. On average, six nodules with a mean diameter of 1.8 cm were seen. Resection of the lesions was performed in all cases. The immunohistochemical and lectin-histochemical examination of the tumors included analysis of the proliferation-associated protein Ki-67, the p53 protein, estrogen and progesterone receptor, sarcolectin as an indicator of the presence of lymphokine macrophage migration inhibitory factor, antibodies and the labeled protein to assess galectin (galactoside-binding animal lectin)-dependent parameters, analysis of tumor vascularization (CD-34), and expression of bcl-2, vimentin, smooth muscle actin, desmin, and keratin. The lesions were characterized by low proliferation activity of 2.9% (measured with Ki-67), frequent hormone receptor expression (8 of the 10 cases presented hormone-specific receptors), low to moderate vascularization compared with metastases from the two uterine sarcomas, remarkable p53 overexpression and frequent expression of the lymphokine, the galectins and accessible binding sites. The median survival of the BML patients was 94 months after excision of the intrapulmonary lesions, and the maximum survival of the two sarcoma patients was 22 months. The results recorded in this patient sample with the methodology applied suggest that benign metastasizing leiomyomas are a slow-growing variant of leiomyosarcoma of the uterus, which becomes clinically apparent at a young age and progresses with low velocity.
Adult↗
Temporal pore formation-mediated egress from macrophages and alveolar epithelial cells by Legionella pneumophila.
Legionella pneumophila does not induce apoptosis in the protozoan host, but induces pore formation-mediated cytolysis after termination of intracellular replication (L.-Y. Gao and Y. Abu Kwaik, Environ. Microbiol. 2:79-90, 2000). In contrast to this single mode of killing of protozoa, we have recently proposed a biphasic model by which L. pneumophila kills macrophages, in which the first phase is manifested through the induction of apoptosis during early stages of the infection, followed by an independent and temporal induction of necrosis during late stages of intracellular replication. Here we show that, similar to the protozoan host, the induction of necrosis and cytolysis of macrophages by L. pneumophila is mediated by the pore-forming toxin or activity. This activity is temporally and maximally expressed only upon termination of bacterial replication and correlates with cytolysis of macrophages and alveolar epithelial cells in vitro. We have identified five L. pneumophila mutants defective in the pore-forming activity. The phagosomes harboring the mutants do not colocalize with the late endosomal or lysosomal marker Lamp-1, and the mutants replicate intracellularly similar to the parental strain. Interestingly, despite their prolific intracellular replication, the mutants are defective in cytotoxicity and are "trapped" within and fail to lyse and egress from macrophages and alveolar epithelial cells upon termination of intracellular replication. However, the mutants are subsequently released from the host cell, most likely due to apoptotic death of the host cell. Data derived from cytotoxicity assays, confocal laser scanning microscopy, and electron microscopy confirm the defect in the mutants to induce necrosis of macrophages and the failure to egress from the host cell. Importantly, the mutants are completely defective in acute lethality (24 to 48 h) to intratracheally inoculated A/J mice. We conclude that the pore-forming activity of L. pneumophila is not required for phagosomal trafficking or for intracellular replication. This activity is expressed upon termination of bacterial replication and is essential to induce cytolysis of infected macrophages to allow egress of intracellular bacteria. In addition, this activity plays a major role in pulmonary immunopathology in vivo.
Animals↗
Morphogenesis, adhesive properties, and antifungal resistance depend on the Pmt6 protein mannosyltransferase in the fungal pathogen candida albicans.
Protein mannosyltransferases (Pmt proteins) initiate O glycosylation of secreted proteins in fungi. We have characterized PMT6, which encodes the second Pmt protein of the fungal pathogen Candida albicans. The residues of Pmt6p are 21 and 42% identical to those of C. albicans Pmt1p and S. cerevisiae Pmt6p, respectively. Mutants lacking one or two PMT6 alleles grow normally and contain normal Pmt enzymatic activities in cell extracts but show phenotypes including a partial block of hyphal formation (dimorphism) and a supersensitivity to hygromycin B. The morphogenetic defect can be suppressed by overproduction of known components of signaling pathways, including Cek1p, Cph1p, Tpk2p, and Efg1p, suggesting a specific Pmt6p target protein upstream of these components. Mutants lacking both PMT1 and PMT6 are viable and show pmt1 mutant phenotypes and an additional sensitivity to the iron chelator ethylenediamine-di(o-hydroxyphenylacetic acid). The lack of Pmt6p significantly reduces adherence to endothelial cells and overall virulence in a mouse model of systemic infection. The results suggest that Pmt6p regulates a more narrow subclass of proteins in C. albicans than Pmt1p, including secreted proteins responsible for morphogenesis and antifungal sensitivities.
Alleles↗
[Advanced nursing education in oncology and palliative care in Northern Germany].
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Education, Nursing, Graduate↗
Use of electrochemical impedance measurements to monitor beta-adrenergic stimulation of bovine aortic endothelial cells.
Due to the high permeability of endothelial cell layers derived from macrovascular vessels, precise determination of their barrier function towards ion movement requires refined experimental techniques. We thus cultured bovine aortic endothelial cells (BAEC) directly on thin gold-film electrodes and measured the electrochemical impedance to study their passive electrical properties in general and during beta-adrenergic stimulation. Impedance spectra (10-2.10(6) Hz) of confluent cell monolayers revealed that the electrical characteristics of the cells can be modelled by a simple resistor-capacitor parallel network. Under control conditions the overall resistance of confluent BAEC monolayers was 3.6+/-0.6 Omega.cm2 (n=30) and the capacitance was 0. 6+/-0.1 microF/cm2. Both quantities are discussed with respect to morphological characteristics of these cells. Stimulation of BAECs with the synthetic beta-adrenoceptor agonist isoproterenol leads to a concentration-dependent, highly specific increase of the cell layer resistance characterized by a concentration for half-maximal response (EC50) of 0.3+/-0.1 microM. The cell layer capacitance, however, remained unaffected. Using impedance measurements at a single frequency, we analysed the response of BAECs to treatment with isoproterenol in comparison with several chemically unrelated compounds known to stimulate the adenosine 3',5'-cyclic monophosphate (cAMP)-dependent signal transduction cascade. These studies confirmed that the enhancement of the cell layer resistance after beta-adrenergic stimulation is mediated by an increase in intracellular cAMP.
Adenylyl Cyclases↗
Pharmacokinetic and clinical evaluation of serious infections in premature and newborn infants under therapy with imipenem/cilastatin.
Efficacy and pharmacokinetic parameters of imipenem/cilastatin (I/C) were investigated in a retrospective evaluation in 104 premature and newborn infants. Patients enrolled in this investigation constituted a particularly high risk group with extreme prematurity, perinatal asphyxia and amnion infection as well as various malformations. In 15 of the 104 infants serum concentrations were measured for drug monitoring and determination of optimal total daily dosage. A total daily dose of 50 mg/kg birth weight for premature and newborn infants divided into two doses led to imipenem peak concentrations of 17.7 mg/l +/- 9.2 mg/l (range: 1.95-38.05) and trough levels were 2.35 mg/l +/-1.02 (range 2.34-10.88) in premature infants. Imipenem peak concentrations of 20.6 +/- 10.8 (range 3.94-32.3) and trough levels of 0.43 +/- 0.17 (range 0.16-0.94) were measured in newborns. The half-life of elimination was 3.3 h and 1.86 h, respectively. Six of the 104 treated patients died, five of them of causes unrelated to infection. Seizures occurred in 8.9% of patients during therapy with I/C compared with 5.8% of a large survey of premature and newborn infants in our intensive care unit (ICU). However, the severity of illness of these two groups cannot be compared. I/C can be expected to constitute effective therapy in premature and newborn infants with serious nosocomial infections even after failure of other broad spectrum antibiotics.
Bacteremia↗
Introduction of apoptosis by high proinsulin and glucose in cultured human umbilical vein endothelial cells is mediated by reactive oxygen species.
There is much evidence that diabetes and hyperglycaemia contribute to the impairment of endothelial function and induce severe changes in the proliferation, the adhesive and synthetic properties of endothelial cells. Induction of apoptosis could represent one mechanism to prevent the new accumulation of those vascular defects and to allow generation of vascular endothelium. In this study, we demonstrate that high concentrations of glucose or proinsulin induce apoptosis in human umbilical endothelial cells by three independent methods (DNA fragmentation, fluorescence activated cell sorting analysis, and morphology). The number of apoptotic cells was increased by glucose (30 mmol/l or proinsulin (100 nmol/l) from less than 10% to about 30%. Activation of protein kinase C (PKC) largely prevented the induction of apoptosis, whereas inhibition of PKC further increased the number of apoptotic cells. Similar changes as induced by glucose were also observed after incubation of the cells with the non-metabolisable 3-O-methylglucose. These findings indicate that hyperglycaemic conditions stimulate the induction of apoptosis in endothelial cells by a mechanism which is independent from the formation of diacylglycerol and the activation of PKC. The induction of apoptosis by the non-metabolisable glucose suggests that formation of oxygen derived radicals by autoxidative processes is involved and may lead to an activation of transcription factors such as nuclear transcription factor-kappaB (NF-kappaB) transferring the activation signal into the nucleus and leading to changes in gene expression necessary for induction of apoptosis.
Apoptosis↗
Migration of the fungal pathogen Candida albicans across endothelial monolayers.
Migration of the fungal pathogen Candida albicans across the endothelial cell layer is considered a prerequisite for the invasion of multiple organs occurring in systemic candidiasis. We developed an experimental system in which C. albicans migrates from a luminal compartment across a monolayer of bovine aortic endothelial cells on a porous filter support to an abluminal compartment. In this system, a C. albicans wild-type strain (ATCC 10261) traverses the endothelial monolayer in a time-, glucose-, and cell concentration-dependent manner. A mutant derivative unable to grow and form hyphae (SGY-243) migrates at a reduced rate. Concomitant to transendothelial migration, the permeability of the endothelial monolayer for dextran diffusion markers is significantly increased. This increase in transendothelial exchange occurs before fungal cells are detectable in the abluminal compartment and is time, glucose, and cell concentration dependent. A mutant strain (hOG301) unable to interact with endothelial cells does not alter endothelial permeability. Thus, transendothelial migration of C. albicans is able to damage the barrier function of an endothelial monolayer. Our experimental system, which reflects key stages of transendothelial migration of C. albicans including adherence and passage across endothelial cells and the extracellular matrix, may be a useful model for comparisons of transendothelial migration characteristics of Candida strains.
Animals↗
NLM extramural program: frequently asked questions.
New and aspiring investigators often ask the same questions of experts as proposals are formulated, written, and submitted to the National Library of Medicine (NLM) for peer review. The NLM's Division of Extramural Programs (EP) provides support to medical libraries, academic medical centers, individuals, and industry through numerous types of grants and contracts. A complex set of processes and procedures is in place and is familiar to established and funded researchers, but to few others. A collection of frequently asked questions (FAQ) and their answers on these issues has been prepared by the Biomedical Library Review Committee (BLRC), a standing advisory group to the NLM that meets three times a year to review and score proposals. The BLRC and two experts on National Institutes of Health (NIH) grants and contracts compiled their advice in an electronic FAQ that has been edited and abridged as an introduction to NLM EP for investigators from medical library science, informatics, and biotechnology. The BLRC expects that if new investigators are able to avoid common mistakes and misconceptions, their proposals will improve in quality and they will be able to spend their time more effectively in proposal preparation.
Biotechnology↗