On the Nonparametric Identification of Nonlinear Simultaneous Equations Models: Comment on B. Brown (1983) and Roehrig (1988)

This note revisits the identification theorems of B. Brown (1983) and Roehrig (1988). We describe an error in the proofs of the main identification theorems in these papers, and provide an important counterexample to the theorems on the identification of the reduced form. Specifically, contrary to the theorems, the reduced form of a nonseparable simultaneous equations model is not identified even under the assumptions of those papers. We conclude the note with a conjecture that it may be possible to use classical exclusion restrictions to recover some of the key implications of the theorems

Dynamic Screening via Intense Laser Radiation and Its Effects on Bulk and Surface Plasma Dispersion Relations

Recent experimentation with excitation of surface plasmons on a gold film in the Kretschmann configuration have shown what appears to be a superconductive effect. Researchers claimed to see the existence of electron pairing during scattering as well as magnetic field repulsion while twisting the polarization of the laser. In an attempt to explain this, they pointed to a combination of electron-electron scattering in external fields as well as dynamic screening via intense laser radiation. This paper expands upon the latter, taking a look at the properties of a dynamic polarization function, its effects on bulk and surface plasmon dispersion relations, and its various consequences

Changes in hyporheic exchange flow following experimental wood removal in a small, low-gradient stream

We investigated the response of hyporheic exchange flow (HEF) to wood removal in a small, low-gradient, gravel bed stream in southeast Alaska using a series of groundwater models built to simulate HEF for the initial conditions immediately after wood removal and 1 month, 2 years, 4 years, and 16 years following wood removal. The models were based on topographic surveys of the stream channel and surrounding floodplain, and surveyed water surface elevations (WSEs) were used to assign stream boundary conditions. Using the groundwater flow model, MODFLOW, and the particle tracking model, MODPATH, we calculated hyporheic exchange fluxes, their residence time distributions, and both longitudinal and plan view spatial patterns of downwelling and upwelling zones. In the first few years, streambed scour and sediment deposition smoothed the streambed and WSE profile, reducing HEF. Also, large contiguous patches of downwelling or upwelling were fragmented, nearly doubling the total number of patches present on the streambed. As the stream continued to adjust to the loss of wood, those trends began to reverse. Accretion of sediment onto alternating bars resulted in better developed pool-riffle morphology, enhanced HEF, and increased residence times and also resulted in downwelling and upwelling zones coalescing into elongated patches along bar margins. This study showed that the hyporheic zone is sensitive to changes in wood loading and that initial changes in HEF resulting from the direct effects of wood removal were contrary to longer-term channel adjustments to changes in wood loading

Prevalence and Clinical Significance of HIV Drug Resistance Mutations by Ultra-Deep Sequencing in Antiretroviral-Naïve Subjects in the CASTLE Study

CASTLE compared the efficacy of atazanavir/ritonavir with lopinavir/ritonavir, each in combination with tenofovir-emtricitabine in ARV-naïve subjects from 5 continents.Determine the baseline rate and clinical significance of TDR mutations using ultra-deep sequencing (UDS) in ARV-naïve subjects in CASTLE.A case control study was performed on baseline samples for all 53 subjects with virologic failures (VF) at Week 48 and 95 subjects with virologic successes (VS) randomly selected and matched by CD4 count and viral load. UDS was performed using 454 Life Sciences/Roche technology.Of 148 samples, 141 had successful UDS (86 subtype B, 55 non-B subtypes). Overall, 30.5% of subjects had a TDR mutation at baseline; 15.6% only had TDR(s) at <20% of the viral population. There was no difference in the rate of TDRs by B (30.2%) or non-B subtypes (30.9%). VF (51) and VS (90) had similar rates of any TDRs (25.5% vs. 33.3%), NNRTI TDRs (11.1% vs.11.8%) and NRTI TDRs (24.4% vs. 25.5%). Of 9 (6.4%) subjects with M184V/I (7 at <20% levels), 6 experienced VF. 16 (11.3%) subjects had multiple TAMs, and 7 experienced VF. 3 (2.1%) subjects had both multiple TAMs+M184V, and all experienced VF. Of 14 (9.9%) subjects with PI TDRs (11 at <20% levels): only 1 experienced virologic failure. The majority of PI TDRs were found in isolation (e.g. 46I) at <20% levels, and had low resistance algorithm scores.Among a representative sample of ARV-naïve subjects in CASTLE, TDR mutations were common (30.5%); B and non-B subtypes had similar rates of TDRs. Subjects with multiple PI TDRs were infrequent. Overall, TDRs did not affect virologic response for subjects on a boosted PI by week 48; however, a small subset of subjects with extensive NRTI backbone TDR patterns experienced virologic failure

CD56negCD16+NK cells are activated mature NK cells with impaired effector function during HIV-1 infection

BACKGROUND: A subset of CD3(neg)CD56(neg)CD16(+) Natural Killer (NK) cells is highly expanded during chronic HIV-1 infection. The role of this subset in HIV-1 pathogenesis remains unclear. The lack of NK cell lineage-specific markers has complicated the study of minor NK cell subpopulations. RESULTS: Using CD7 as an additional NK cell marker, we found that CD3(neg)CD56(neg)CD16(+) cells are a heterogeneous population comprised of CD7(+) NK cells and CD7(neg) non-classical myeloid cells. CD7(+)CD56(neg)CD16(+) NK cells are significantly expanded in HIV-1 infection. CD7(+)CD56(neg)CD16(+) NK cells are mature and express KIRs, the C-type lectin-like receptors NKG2A and NKG2C, and natural cytotoxicity receptors similar to CD7(+)CD56(+)CD16(+) NK cells. CD7(+)CD56(neg) NK cells in healthy donors produced minimal IFNγ following K562 target cell or IL-12 plus IL-18 stimulation; however, they degranulated in response to K562 stimulation similar to CD7(+)CD56(+) NK cells. HIV-1 infection resulted in reduced IFNγ secretion following K562 or cytokine stimulation by both NK cell subsets compared to healthy donors. Decreased granzyme B and perforin expression and increased expression of CD107a in the absence of stimulation, particularly in HIV-1-infected subjects, suggest that CD7(+)CD56(neg)CD16(+) NK cells may have recently engaged target cells. Furthermore, CD7(+)CD56(neg)CD16(+) NK cells have significantly increased expression of CD95, a marker of NK cell activation. CONCLUSIONS: Taken together, CD7(+)CD56(neg)CD16(+) NK cells are activated, mature NK cells that may have recently engaged target cells

A Multi-Institutional Analysis of Insurance Status as a Predictor of Morbidity Following Breast Reconstruction.

BACKGROUND: Although recent literature suggests that patients with Medicaid and Medicare are more likely than those with private insurance to experience complications following a variety of procedures, there has been limited evaluation of insurance-based disparities in reconstructive surgery outcomes. Using a large, multi-institutional database, we sought to evaluate the potential impact of insurance status on complications following breast reconstruction. METHODS: We identified all breast reconstructive cases in the 2008 to 2011 Tracking Operations and Outcomes for Plastic Surgeons clinical registry. Propensity scores were calculated for each case, and insurance cohorts were matched with regard to demographic and clinical characteristics. Outcomes of interest included 15 medical and 13 surgical complications. RESULTS: Propensity-score matching yielded 493 matched patients for evaluation of Medicaid and 670 matched patients for evaluation of Medicare. Overall complication rates did not significantly differ between patients with Medicaid or Medicare and those with private insurance (P = 0.167 and P = 0.861, respectively). Risk-adjusted multivariate regressions corroborated this finding, demonstrating that Medicaid and Medicare insurance status does not independently predict surgical site infection, seroma, hematoma, explantation, or wound dehiscence (all P \u3e 0.05). Medicaid insurance status significantly predicted flap failure (odds ratio = 3.315, P = 0.027). CONCLUSIONS: This study is the first to investigate the differential effects of payer status on outcomes following breast reconstruction. Our results suggest that Medicaid and Medicare insurance status does not independently predict increased overall complication rates following breast reconstruction. This finding underscores the commitment of the plastic surgery community to providing consistent care for patients, irrespective of insurance status

Impact of Postoperative Antibiotic Prophylaxis Duration on Surgical Site Infections in Autologous Breast Reconstruction.

BACKGROUND: Although some surgeons prescribe prolonged postoperative antibiotics after autologous breast reconstruction, evidence is lacking to support this practice. We used the Tracking Operations and Outcomes for Plastic Surgeons database to evaluate the association between postoperative antibiotic duration and the rate of surgical site infection (SSI) in autologous breast reconstruction. STUDY DESIGN: The intervention of interest for this study was postoperative duration of antibiotic prophylaxis: either discontinued 24 hours after surgery or continued beyond 24 hours. The primary outcome variable of interest for this study was the presence of SSI within 30 days of autologous breast reconstruction. Cohort characteristics and 30-day outcomes were compared using χ and Fischer exact tests for categorical variables and Student t tests for continuous variables. Multivariate logistic regression was used to control for confounders. RESULTS: A total of 1036 patients met inclusion criteria for our study. Six hundred fifty-nine patients (63.6%) received antibiotics for 24 hours postoperatively, and 377 patients (36.4%) received antibiotics for greater than 24 hours. The rate of SSI did not differ significantly between patients given antibiotics for only 24 hours and those continued on antibiotics beyond the 24-hour postoperative time period (5.01% vs 2.92%, P = 0.109). Furthermore, antibiotic duration was not predictive of SSI in multivariate regression modeling. CONCLUSIONS: We did not find a statistically significant difference in the rate of SSI in patients who received 24 hours of postoperative antibiotics compared to those that received antibiotics for greater than 24 hours. These findings held for both purely autologous reconstruction as well as latissimus dorsi reconstruction in conjunction with an implant. Thus, our study does not support continuation of postoperative antibiotics beyond 24 hours after autologous breast reconstruction

A Multi-institutional Analysis of Insurance Status as a Predictor of Morbidity Following Breast Reconstruction

Background: Although recent literature suggests that patients with Medicaid and Medicare are more likely than those with private insurance to experience complications following a variety of procedures, there has been limited evaluation of insurance-based disparities in reconstructive surgery outcomes. Using a large, multi-institutional database, we sought to evaluate the potential impact of insurance status on complications following breast reconstruction. Methods: We identified all breast reconstructive cases in the 2008 to 2011 Tracking Operations and Outcomes for Plastic Surgeons clinical registry. Propensity scores were calculated for each case, and insurance cohorts were matched with regard to demographic and clinical characteristics. Outcomes of interest included 15 medical and 13 surgical complications. Results: Propensity-score matching yielded 493 matched patients for evaluation of Medicaid and 670 matched patients for evaluation of Medicare. Overall complication rates did not significantly differ between patients with Medicaid or Medicare and those with private insurance (P = 0.167 and P = 0.861, respectively). Risk-adjusted multivariate regressions corroborated this finding, demonstrating that Medicaid and Medicare insurance status does not independently predict surgical site infection, seroma, hematoma, explantation, or wound dehiscence (all P > 0.05). Medicaid insurance status significantly predicted flap failure (odds ratio = 3.315, P = 0.027). Conclusions: This study is the first to investigate the differential effects of payer status on outcomes following breast reconstruction. Our results suggest that Medicaid and Medicare insurance status does not independently predict increased overall complication rates following breast reconstruction. This finding underscores the commitment of the plastic surgery community to providing consistent care for patients, irrespective of insurance status