The Montreal Neurological Institute: training of the first African-American neurosurgeons

BACKGROUND: Since its inception in 1934 by the legendary Dr. Wilder Penfield, the Montreal Neurological Institute (MNI) has provided world-renowned instruction in neurosurgery and related neurosciences, training many of the most prominent figures in the history of neurosurgery. Less well known is the role of the MNI in training the first African-American board-certified neurosurgeons. METHODS: A comprehensive review of pertinent modern and historical records spanning the past century was performed. RESULTS: From 1947-1965, the MNI trained the first African-American board-certified neurosurgeon, and three of the first four. The first, Dr. Clarence Greene, Sr., trained at MNI from 1947-1949. The next, Dr. Jesse Barber, Jr., trained at MNI from 1958-1961. Like Greene, Barber received his MD from the Howard University College of Medicine, was on the general surgery faculty at Howard before training at MNI under Penfield and returned to Howard following his training. The third, Dr. Lloyd Dayes, matriculated at MNI in 1960 after receiving his MD from the Loma Linda University School of Medicine and trained from 1961-1965 under Dr. Theodore Rasmussen, after which he returned to Loma Linda. Greene, Barber and Dayes were certified by the American Board of Neurological Surgery in 1953, 1963 and 1967, respectively, as the first, third and fourth African-American neurosurgeons. CONCLUSION: The willingness of the world-renowned MNI to train the first African-American neurosurgeons during a time of intense racial segregation in the United States played a major role in enabling subsequent African Americans to enter and enhance the field of neurosurgery.     

Health insurance status and type associated with varying levels of glycemic control in the US: The multi-ethnic study of atherosclerosis (MESA)

AimsTo investigate associations of health insurance with measures of glucose metabolism, and whether associations vary by diabetes status or insurance type.MethodsCross-sectional analysis of baseline data from the Multi-Ethnic Study of Atherosclerosis. Cohort a priori stratified by age <65 (N = 3,665) and ≥65 years (N = 2,924). Multivariable linear and logistic regression assessed associations between insurance and fasting glucose, HOMA-IR, and prevalent diabetes, controlling for relevant confounders, including age, sex, race/ethnicity, income, and education.ResultsIn participants <65, compared to uninsured, having any insurance was associated with lower fasting glucose in participants with diabetes (Mean Difference = ?20.4 mg/dL, P = 0.01), but not in participants without diabetes. Compared to Private insurance, uninsured participants had higher fasting glucose (Mean Difference = 3.8 mg/dL, P = 0.03), while participants with Medicaid had higher HOMA-IR (Mean Difference = 3.5 mg/dL, P < 0.01). In participants ≥65, compared to Private insurance, uninsured participants (Mean Difference = 7.5 mg/dL, P = 0.02), and participants with Medicaid only (Mean Difference = 19.9 mg/dL, P < 0.01) or Medicare + Medicaid (Mean Difference = 5.2 mg/dL, P = 0.03) had higher fasting glucose.ConclusionsIn this large multiethnic cohort, having any insurance was associated with significantly lower fasting glucose for individuals with diabetes. Levels of fasting glucose and insulin resistance varied across different insurance types.     

Comparison of ventricular arrhythmia induction with use of an indwelling electrode catheter and a newly inserted catheter

Two methods of serial electrophysiologic testing are in widespread use. Most commonly, the electrode catheter is removed after each study and a new catheter reinserted through the femoral vein for every subsequent test. An alternative method employs an electrode catheter that remains in place during several days of serial testing. Little is known about differences between these two methods with respect to the likelihood of induction of arrhythmia or the frequency of complications. To determine whether inducibility of sustained arrhythmia is altered or if the frequency of complications is unacceptably high with use of an indwelling catheter, a prospective randomized study was conducted in 78 patients. Each patient underwent baseline testing, several days of electropharmacologic testing with an indwelling catheter, a 24 h drug elimination period and placement of a new electrode catheter. Ventricular stimulation studies were then performed in each patient with both the indwelling and new electrode catheters. No differences were found between the indwelling and new catheter tests with respect to induction of arrhythmia, number of extrastimuli required to induce arrhythmia, rate of arrhythmia or requirement for cardioversion. Ventricular pacing thresholds were higher and effective refractory periods were slightly longer when measured with the indwelling catheter. Complications related to the 156 catheter insertions included two that may have been related to the indwelling catheter (one episode of staphylococcal sepsis and one presumed pulmonary embolism) and four that were related to invasive procedures (pneumothorax in all). There were no long-term adverse sequelae of these complications.(ABSTRACT TRUNCATED AT 250 WORDS)     

Administration of pegylated recombinant human megakaryocyte growth and development factor to humans stimulates the production of functional platelets that show no evidence of in vivo activation

This report describes the effect of pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) on platelet production and platelet function in humans. Subjects with advanced solid tumors received PEG-rHuMGDF daily for up to 10 days. There was no increase in circulating platelet count at doses of 0.03 or 0.1 microgram/kg/d by day 12 of study. At doses of 0.3 and 1.0 microgram/kg/d there was a threefold median increase (maximum 10-fold) in platelet count by day 16. The platelets produced in vivo in response to PEG-rHuMGDF showed unchanged aggregation and adenosine triphosphate (ATP)-release responses in in vitro assays. Tests included aggregation and release of ATP in response to adenosine diphosphate (ADP) (10, 5, 2.5, and 1.25 mumol/L), collagen (2 micrograms/mL), thrombin-receptor agonist peptide (TRAP, 10 mumol/L) and ristocetin (1.5 mg/mL). Administration of aspirin to an individual with platelet count of 1,771 x 10(3)/L resulted in the typical aspirin-induced ablation of the normal aggregation and ATP-release response to stimulation with arachidonic acid (0.5 mg/mL), collagen, and ADP (2.5 and 1.25 mumol/L). There was no change in the expression of the platelet-surface activation marker CD62P (P-selectin) nor induction of the fibrinogen binding site on glycoprotein IIb/IIIa as reported by the monoclonal antibody, D3GP3. An elevation of reticulated platelets was evident after 3 days of treatment with PEG-rHuMGDF and preceded the increase in circulating platelet count by 5 to 8 days; this reflected the production of new platelets in response to PEG-rHuMGDF. At later time points, the mean platelet volume (MPV) decreased in a manner inversely proportional to the platelet count. Levels of plasma glycocalicin, a measure of platelet turnover, rose 3 days after the initial increase in the peripheral platelet count. The level of plasma glycocalicin was proportional to the total platelet mass, suggesting that platelets generated in response to PEG-rHuMGDF were not more actively destroyed. Thus, the administration of PEG-rHuMGDF, to humans, increased the circulating platelet count and resulted in fully functional platelets, which showed no detectable increase in reactivity nor alteration in activation status.     

B220- bone marrow progenitor cells from New Zealand black autoimmune mice exhibit an age-associated decline in Pre-B and B-cell generation

New Zealand Black (NZB) autoimmune mice exhibit progressive, age- dependent reduction in bone marrow pre-B cells. To ascertain the capacity of NZB bone marrow B220- cells to generate pre-B cells in a supportive environment, B-lineage (B220+) cell-depleted and T-cell- depleted bone marrow cells from NZB mice at 1 to 3, 6, and 10 to 11 months of age were adoptively transferred into irradiated (200R) C.B17 severe combined immunodeficient (SCID) mice. Bone marrow pre-B cells (sIgM- CD43[S7]- B220+) were assessed 3 and 10 weeks posttransfer. Pre- B cells and B cells were reconstituted in SCID recipients of older NZB progenitor cells by 10 weeks posttransplant, in contrast to the very low numbers of pre-B cells present in the donor bone marrow. However, B220- bone marrow progenitor cells from greater than 10-month-old NZB donors were deficient in the reconstitution of both pre-B and B cells in SCID recipients at 3 weeks post-transfer. This reflected a slower kinetics of repopulation, because older NZB-->SCID recipients had numbers of both pre-B and B cells similar to recipients of young NZB progenitor cells by 10 weeks posttransplant. Adoptive transfer of equal mixtures of BALB/c and older NZB bone marrow B220- progenitor cells into irradiated C.B17 SCID recipients failed to demonstrate active suppression. These results suggest that, with age, NZB bone marrow has reduced numbers and/or function of early B220- B-lineage progenitors. Consistent with this hypothesis, B220- bone marrow cells from older NZB mice were deficient in progenitors capable of yielding interleukin-7 (IL-7) responsive pre-B cells in vitro on stimulation with the pre-B- cell potentiating factor, insulin-like growth factor 1 (IGF-1).     

The Affordable Care Act and Emergency Care

The Affordable Care Act (ACA) will have far-reaching effects on the way health care is designed and delivered. Several elements of the ACA will directly affect both demand for ED care and expectations for its role in providing coordinated care. Hospitals will need to employ strategies to reduce ED crowding as the ACA expands insurance coverage. Discussions between EDs and primary care physicians about their respective roles providing acute unscheduled care would promote the goals of the ACA.The Affordable Care Act (ACA) focuses on improving access and quality by expanding insurance coverage, using payment reform strategies, and increasing quality reporting.1 In the ACA, hospital-based emergency departments (EDs) are referenced as places to be avoided and reduced; no new payment models focus on ED care, and there are no plans to broadly address ED-specific quality through new measurement programs.Promoting value in ED care needs to be a greater focus for policymakers as the ACA is implemented. Emergency departments play a central role in health care delivery as the staging area for the ill and injured, and as an always-available resource for unscheduled care. Emergency department physicians constitute less than 5% of the US physician workforce, yet manage 28% of acute care encounters.2 Historically, the need for EDs arose from increases in vehicular trauma that accompanied the expansion of the Interstate Highway System in the 1960s.3 However, EDs also quickly became providers of low acuity unscheduled care as well.4 The Emergency Medical Treatment and Active Labor Act legislation passed in 1986 institutionalized EDs as provider of last resort for all, regardless of their ability to pay. Emergency departments have replaced the community physician’s office as the primary source for hospital admissions and provide a safety net for the uninsured, underinsured, and medically disenfranchised.5,6Several elements of the ACA—the insurance expansion, patient-centered medical homes, accountable care organizations, and bundled payments—will directly affect both demand for ED care and expectations for its role in providing coordinated care. We explore these effects and suggest some practical ways that EDs can be better integrated into these efforts.     

鸟氨酸脱羧酶的生理病理特点及其药物研究概况

鸟氨酸脱羧酶(ornithinedecarboxylase,ODC)是多胺代谢中的关键酶,广泛存在于人体和动物各组织细胞内,其中对肠细胞的增生、移行和分化起重要作用.机体调节因素比较复杂.在黏膜损伤性疾病及某些癌前病变等细胞大量增生的病理情况下ODC的表达发生改变,可以作为这些疾病分期、预后及药物作用靶点或疗效的指标.寻找对ODC有作用的药物对于治疗其相关疾病是非常有意义的.     

Thrombospondin mediates the cytoadherence of Plasmodium falciparum- infected red cells to vascular endothelium in shear flow conditions

Cerebral malaria is thought to involve specific attachment of Plasmodium falciparum-infected knobby red cells to venular endothelium. The nature of surface ligands on host endothelial cells that may mediate cytoadherence is poorly understood. We have investigated the effects of soluble thrombospondin, rabbit antiserum raised against thrombospondin, and human immune serum on cytoadherence of parasitized erythrocytes in ex vivo mesocecum vasculature. Preincubation of infected red cells with soluble thrombospondin or human immune serum inhibits binding of infected red cells to rat venular endothelium. Infusion of the microcirculatory preparation with rabbit antithrombospondin antibodies before perfusion of parasitized erythrocytes also resulted in decreased cytoadherence. In addition, incubation of infected cells with human immune sera obtained from malaria patients significantly inhibited the observed cytoadherence. Our results indicate that thrombospondin mediates binding of infected red cells to venular endothelium and may thus be involved in the pathogenesis of cerebral malaria.