Moderating influences on the firm's strategic orientation-performance relationship

This paper is focused on the factors that moderate the relationship between firm's strategic orientation and performance in small and medium-sized firms. Much prior research has focused simply on identifying environmental conditions conducive to the effectiveness of the strategic orientation approach. However, recent research has called for studies focused on investigating internal moderators of the strategic orientation-performance relationship. As a result, we propose a contingency framework, considering how corporate and competitive strategies, top management characteristics, and environmental conditions may moderate this relationship. Based on a survey of 295 small and medium sized enterprises pertaining to seven manufacturing sectors, our study shows that the positive influence of firm's strategic orientation may be moderated by the environment conditions, the previous experience of top management team, and the corporate and competitive strategies developed by the firm

Diabetes, atherosclerosis, and stenosis by AI

OBJECTIVEThis study evaluates the relationship between atherosclerotic plaque characteristics (APCs) and angiographic stenosis severity in patients with and without diabetes. Whether APCs differ based on lesion severity and diabetes status is unknown.RESEARCH DESIGN AND METHODSWe retrospectively evaluated 303 subjects from the Computed TomogRaphic Evaluation of Atherosclerotic Determinants of Myocardial IsChEmia (CREDENCE) trial referred for invasive coronary angiography with coronary computed tomographic angiography (CCTA) and classified lesions as obstructive (≥50% stenosed) or nonobstructive using blinded core laboratory analysis of quantitative coronary angiography. CCTA quantified APCs, including plaque volume (PV), calcified plaque (CP), noncalcified plaque (NCP), low-density NCP (LD-NCP), lesion length, positive remodeling (PR), high-risk plaque (HRP), and percentage of atheroma volume (PAV; PV normalized for vessel volume). The relationship between APCs, stenosis severity, and diabetes status was assessed.RESULTSAmong the 303 patients, 95 (31.4%) had diabetes. There were 117 lesions in the cohort with diabetes, 58.1% of which were obstructive. Patients with diabetes had greater plaque burden (P = 0.004). Patients with diabetes and nonobstructive disease had greater PV (P = 0.02), PAV (P = 0.02), NCP (P = 0.03), PAV NCP (P = 0.02), diseased vessels (P = 0.03), and maximum stenosis (P = 0.02) than patients without diabetes with nonobstructive disease. APCs were similar between patients with diabetes with nonobstructive disease and patients without diabetes with obstructive disease. Diabetes status did not affect HRP or PR. Patients with diabetes had similar APCs in obstructive and nonobstructive lesions.CONCLUSIONSPatients with diabetes and nonobstructive stenosis had an association to similar APCs as patients without diabetes who had obstructive stenosis. Among patients with nonobstructive disease, patients with diabetes had more total PV and NCP.Cardiolog

Viral coinfections in hospitalized coronavirus disease 2019 patients recruited to the international severe acute respiratory and emerging infections consortium WHO clinical characterisation protocol UK study

Background We conducted this study to assess the prevalence of viral coinfection in a well characterized cohort of hospitalized coronavirus disease 2019 (COVID-19) patients and to investigate the impact of coinfection on disease severity. Methods Multiplex real-time polymerase chain reaction testing for endemic respiratory viruses was performed on upper respiratory tract samples from 1002 patients with COVID-19, aged <1 year to 102 years old, recruited to the International Severe Acute Respiratory and Emerging Infections Consortium WHO Clinical Characterisation Protocol UK study. Comprehensive demographic, clinical, and outcome data were collected prospectively up to 28 days post discharge. Results A coinfecting virus was detected in 20 (2.0%) participants. Multivariable analysis revealed no significant risk factors for coinfection, although this may be due to rarity of coinfection. Likewise, ordinal logistic regression analysis did not demonstrate a significant association between coinfection and increased disease severity. Conclusions Viral coinfection was rare among hospitalized COVID-19 patients in the United Kingdom during the first 18 months of the pandemic. With unbiased prospective sampling, we found no evidence of an association between viral coinfection and disease severity. Public health interventions disrupted normal seasonal transmission of respiratory viruses; relaxation of these measures mean it will be important to monitor the prevalence and impact of respiratory viral coinfections going forward

Delayed mucosal anti-viral responses despite robust peripheral inflammation in fatal COVID-19

Background While inflammatory and immune responses to SARS-CoV-2 infection in peripheral blood are extensively described, responses at the upper respiratory mucosal site of initial infection are relatively poorly defined. We sought to identify mucosal cytokine/chemokine signatures that distinguished COVID-19 severity categories, and relate these to disease progression and peripheral inflammation. Methods We measured 35 cytokines and chemokines in nasal samples from 274 patients hospitalised with COVID-19. Analysis considered the timing of sampling during disease, as either the early (0-5 days post-symptom onset) or late (6-20 days post-symptom onset). Results Patients that survived severe COVID-19 showed IFN-dominated mucosal immune responses (IFN-γ, CXCL10 and CXCL13) early in infection. These early mucosal responses were absent in patients that would progress to fatal disease despite equivalent SARS-CoV-2 viral load. Mucosal inflammation in later disease was dominated by IL-2, IL-10, IFN-γ, and IL-12p70, which scaled with severity but did not differentiate patients who would survive or succumb to disease. Cytokines and chemokines in the mucosa showed distinctions from responses evident in the peripheral blood, particularly during fatal disease. Conclusions Defective early mucosal anti-viral responses anticipate fatal COVID-19 but are not associated with viral load. Early mucosal immune responses may define the trajectory of severe COVID-19

Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease

One in ten severe acute respiratory syndrome coronavirus 2 infections result in prolonged symptoms termed long coronavirus disease (COVID), yet disease phenotypes and mechanisms are poorly understood1. Here we profiled 368 plasma proteins in 657 participants ≥3 months following hospitalization. Of these, 426 had at least one long COVID symptom and 233 had fully recovered. Elevated markers of myeloid inflammation and complement activation were associated with long COVID. IL-1R2, MATN2 and COLEC12 were associated with cardiorespiratory symptoms, fatigue and anxiety/depression; MATN2, CSF3 and C1QA were elevated in gastrointestinal symptoms and C1QA was elevated in cognitive impairment. Additional markers of alterations in nerve tissue repair (SPON-1 and NFASC) were elevated in those with cognitive impairment and SCG3, suggestive of brain–gut axis disturbance, was elevated in gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2-specific immunoglobulin G (IgG) was persistently elevated in some individuals with long COVID, but virus was not detected in sputum. Analysis of inflammatory markers in nasal fluids showed no association with symptoms. Our study aimed to understand inflammatory processes that underlie long COVID and was not designed for biomarker discovery. Our findings suggest that specific inflammatory pathways related to tissue damage are implicated in subtypes of long COVID, which might be targeted in future therapeutic trials

Screen-printing of 1720 and 7059 glass insulating bonds for the radioisotopic thermoelectric generator

As part of the RTG fabrication sequence, Si/Ge and Si/Ge-glass substrates are coated with Corning 1720 and 7059 glass by a screen-printing process. A slurry of glass, pine oil, and terpinol is printed, followed by a burnout of the organic matter in oxygen at 500 deg C. It has been determined from overall fabrication considerations that there should be sufficient glass present to yield a fused-glass thickness of 1.2 to 1.4 mils. Glass content of the slurry, screen size, squeegee pressure, and breakaway distance are the important parameters affecting the amount of glass printed. Less variability in glass thickness is experienced when the screen contacts the substrate during printing. This occurs at higher squeegee pressures. The desired glass thickness is achieved by adjusting the glass content of the slurry to the screen mesh size, i.e., less glass is needed for an 80-mesh screen than for a 105mesh screen. Not all of the slurry is retained on the substrate during printing; the fraction adhering to the screen is a function of the breakaway distance. Moderate slurry viscosity and temperature changes during screen printing have only minor effects on the thickness of the glass deposited. Routine printing of 1720 and 7059 glass slurries with 65- and 70-% glass have consistently yielded glass thicknesses between 1.2 and 1.4 mils. (auth

Filament formation on printed wiring boards

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Effect of high-moisture environments on printed-wiring-board insulation

The use of high impedance circuitry and narrow conductor separations in current designs is generating increasing concern for the insulation resistance between conductive elements especially those used in high moisture environments. This concern is multiplied by the expanding use of electronic devices in a greater variety of environments and the desire for less heat generation within the device. The high insulation resistance of a dry printed circuit board can be degraded in high moisture environments by electrolytic conducting paths and/or electronic conducting filament growths between conductive elements. The essential ingredients for resistance degradation are bias and a moisture path linking the conductors. Ions derived from the interaction of moisture with the material on or in the substrate enhance the electrolytic conduction. This material can be residue from processing and handling, air borne contaminate, or leachable constituents from the substrate. A moisture path can form from atmospheric condensate accompanying a temperature change, i.e., dew, or from water adsorption on hydrophillic sites or hydroscopic contaminants on the surface. Methods for preventing the resistance degradation of printed circuit boards, e.g., cleaning, heating, using sealed enclosures, and board surface treatments with water repellants and coatings are discussed. (LCL