ABSTRACT
BACKGROUND: Passive-dynamic ankle-foot orthoses (PD-AFOs) are often prescribed to address plantar flexor weakness during gait, which is commonly observed after stroke. However, limited evidence is available to inform the prescription guidelines of PD-AFO bending stiffness. This study assessed the extent to which PD-AFOs customized to match an individual's level of plantar flexor weakness influence walking function, as compared to No AFO and their standard of care (SOC) AFO. METHODS: Mechanical cost-of-transport, self-selected walking speed, and key biomechanical variables were measured while individuals greater than six months post-stroke walked with No AFO, with their SOC AFO, and with a stiffness-customized PD-AFO. Outcomes were compared across these conditions using a repeated measures ANOVA or Friedman test (depending on normality) for group-level analysis and simulation modeling analysis for individual-level analysis. RESULTS: Twenty participants completed study activities. Mechanical cost-of-transport and self-selected walking speed improved with the stiffness-customized PD-AFOs compared to No AFO and SOC AFO. However, this did not result in a consistent improvement in other biomechanical variables toward typical values. In line with the heterogeneous nature of the post-stroke population, the response to the PD-AFO was highly variable. CONCLUSIONS: Stiffness-customized PD-AFOs can improve the mechanical cost-of-transport and self-selected walking speed in many individuals post-stroke, as compared to No AFO and participants' standard of care AFO. This work provides initial efficacy data for stiffness-customized PD-AFOs in individuals post-stroke and lays the foundation for future studies to enable consistently effective prescription of PD-AFOs for patients post-stroke in clinical practice. TRIAL REGISTRATION: NCT04619043.
Subject(s)
Foot Orthoses , Stroke Rehabilitation , Walking Speed , Humans , Male , Female , Middle Aged , Stroke Rehabilitation/instrumentation , Stroke Rehabilitation/methods , Walking Speed/physiology , Aged , Biomechanical Phenomena , Stroke/complications , Stroke/physiopathology , Ankle/physiology , Walking/physiology , Gait Disorders, Neurologic/rehabilitation , Gait Disorders, Neurologic/etiologyABSTRACT
STUDY DESIGN: Retrospective review of a prospectively-collected multicenter database. OBJECTIVES: The objective of this study was to determine optimal strategies in terms of focal angular correction and length of proximal extension during revision for PJF. METHODS: 134 patients requiring proximal extension for PJF were analyzed in this study. The correlation between amount of proximal junctional angle (PJA) reduction and recurrence of proximal junctional kyphosis (PJK) and/or PJF was investigated. Following stratification by the degree of PJK correction and the numbers of levels extended proximally, rates of radiographic PJK (PJA >28° & ΔPJA >22°), and recurrent surgery for PJF were reported. RESULTS: Before revision, mean PJA was 27.6° ± 14.6°. Mean number of levels extended was 6.0 ± 3.3. Average PJA reduction was 18.8° ± 18.9°. A correlation between the degree of PJA reduction and rate of recurrent PJK was observed (r = -.222). Recurrent radiographic PJK (0%) and clinical PJF (4.5%) were rare in patients undergoing extension ≥8 levels, regardless of angular correction. Patients with small reductions (<5°) and small extensions (<4 levels) experienced moderate rates of recurrent PJK (19.1%) and PJF (9.5%). Patients with large reductions (>30°) and extensions <8 levels had the highest rate of recurrent PJK (31.8%) and PJF (16.0%). CONCLUSION: While the degree of focal PJK correction must be determined by the treating surgeon based upon clinical goals, recurrent PJK may be minimized by limiting reduction to <30°. If larger PJA correction is required, more extensive proximal fusion constructs may mitigate recurrent PJK/PJF rates.
ABSTRACT
BACKGROUND: Bowel dilation and bowel wall thickness are common prenatal ultrasound measurements for fetuses with gastroschisis. Data regarding antenatal sonographic bowel findings and postnatal outcomes are conflicting. Our objective was to evaluate the impact of in utero bowel measurements on perinatal outcomes in gastroschisis pregnancies. METHODS: Retrospective cohort study of 116 pregnancies complicated by gastroschisis between 2011 and 2020. We reviewed ultrasounds documenting fetal bowel measurements. To evaluate the association of these measurements with antepartum and delivery outcomes, we ran logistic and linear models using generalized estimating equations. RESULTS: Eleven perinatal outcomes reached statistical significance, although with minimal clinical impact given small magnitude of effect. Intra-abdominal bowel dilation was associated with a 0.5 week decrease in delivery gestational age (GA) (95% CI -0.07, -0.03) and a 6.93âg increase in birth weight (95% CI 1.54, 28.73). Intra-abdominal bowel wall thickness was associated with later GA of non-stress test (NST) start of 0.22 weeks (95% CI 0.07, 0.37), increased delivery GA of 0.08 weeks (95% CI 0.02, 0.15), 0.006 decrease in umbilical artery (UA) pH (95% CI -0.009, -0.003), 0.26 increase in UA base deficit (95% CI 0.09, 0.43), and decreased odds of cesarean delivery (ORâ=â0.83, 95% CI 0.70, 0.99). Extra-abdominal bowel wall thickness was associated with a 0.1 increase in UA base deficit (95% CI 0.02, 0.19) and a 0.05 increase in 5-min APGAR score (95% CI 0.01, 0.09). Stomach cross-section was associated with a 0.01 week decrease in delivery GA (95% CI -0.02, -0.001) and increased odds of receiving betamethasone (ORâ=â1.02, 95% CI 1.01, 1.04). CONCLUSIONS: In utero bowel characteristics reached statistical significance for several outcomes, but with minimal meaningful clinical differences in outcomes.
Subject(s)
Gastroschisis , Female , Humans , Pregnancy , Dilatation, Pathologic/complications , Gastroschisis/diagnostic imaging , Gestational Age , Intestines/diagnostic imaging , Retrospective Studies , Ultrasonography , Ultrasonography, PrenatalABSTRACT
During human locomotion, each limb performs step-to-step work on the body center of mass to maintain forward walking. This energy exchange relies on physiological mechanisms which are altered or impaired in transfemoral prosthesis users (TFPUs). Exploring step-to-step energy exchange modifications displayed by TFPUs at greater walking speeds may provide insight into their means for improving gait efficiency. The primary aim of this study was to characterize the effects of walking speed on mechanical work in unilateral TFPUs. The secondary aim assessed the effect of prosthetic knee (microprocessor, mechanical passive) on limb collision work. Twenty-five TFPUs walked with their customary prosthesis on a split-belt instrumented treadmill at eight speeds (0.55-1.53 m/s range), and collision, midstance, and push-off work were calculated for each limb. TFPUs displayed a significant (p < 0.001) bilateral increase in collision work with increased walking speed, but midstance and push-off work increased only for the sound limb and remained nearly constant for the prosthetic limb. TFPUs displayed significantly (p < 0.001) less push-off work generated by the prosthetic limb across all speeds. A microprocessor knee was associated with reduced sound limb collision work across speeds with the peak (negative) power being significantly greater for mechanical knees (p = 0.032). Results suggest that TFPU gait inefficiency may be related to a near complete loss of energy transfer on the prosthetic limb, relying on the sound limb to drive energy changes. Such reliance emphasizes need for attention to the long-term effects on sound limb health and possible benefit of microprocessor knees to offset that impact.
Subject(s)
Amputees , Artificial Limbs , Knee Prosthesis , Biomechanical Phenomena , Gait/physiology , Humans , Prosthesis Design , Walking , Walking SpeedABSTRACT
Tar spot is a fungal disease complex of corn that has been destructive and yield limiting in Central and South America for nearly 50 years. Phyllachora maydis, the causal agent of tar spot, is an emerging corn pathogen in the United States, first reported in 2015 from major corn producing regions of the country. The tar spot disease complex putatively includes Monographella maydis (syn. Microdochium maydis), which increases disease damage through the development of necrotic halos surrounding tar spot lesions. These necrotic halos, termed "fish-eye" symptoms, have been identified in the United States, though Monographella maydis has not yet been confirmed. A recent surge in disease severity and loss of yield attributed to tar spot in the United States has led to increased attention and expanded efforts to understand the disease complex and how to manage it. In this study, next-generation sequencing of the internal transcribed spacer-1 (ITS1) ribosomal DNA was used to identify fungal taxa that distinguish tar spot infections with or without fish-eye symptoms. Fungal communities within tar spot only lesions were significantly different from communities having fish-eye symptoms. Two low abundance OTUs were identified as Microdochium sp., however, neither were associated with fish-eye symptom development. Interestingly, a single OTU was found to be significantly more abundant in fish-eye lesions compared to tar spot lesions and had a 91% ITS1 identity to Neottiosporina paspali. In addition, the occurrence of this OTU was positively associated with Phyllachora maydis fish-eye symptom networks, but not in tar spot symptom networks. Neottiosporina paspali has been reported to cause necrotic lesions on various monocot grasses. Whether the related fungus we detected is part of the tar-spot complex of corn and responsible for fish-eye lesions remains to be tested. Alternatively, many OTUs identified as Phyllachora maydis, suggesting that different isolate genotypes may be capable of causing both tar spot and fish-eye symptoms, independent of other fungi. We conclude that Monographella maydis is not required for fish-eye symptoms in tar spot of corn.
ABSTRACT
BACKGROUND: Hepatic artery thrombosis (HAT) remains among the leading causes of early graft loss after liver transplantation. Our transplant center began using universal aspirin prophylactic therapy immediately posttransplantation in 2007. The aim of this study was to determine the safety and efficacy of early aspirin therapy on clinical outcomes. METHODS: This large-scale, cross-sectional analysis included all adult liver transplantations performed between 2000 and 2009. Pediatric and multiorgan transplants were excluded. Patients were grouped and compared based on whether they received early initiation of aspirin 325 mg PO daily posttransplantation. RESULTS: A total of 541 adult liver transplantations occurred during the study period; 439 had complete documentation and were analyzed. Clinical outcomes show aspirin patients had similar rates of early and late HAT, but had significantly lower early HAT, defined as HAT occurring within the first 30 days posttransplant, leading to graft loss. Other clinical outcomes were similar between groups including bleeding events and wound complications. CONCLUSIONS: Immediate initiation of aspirin therapy after liver transplantation may reduce the rate of HAT leading to early graft loss, without increasing bleeding or other complication rates.
Subject(s)
Aspirin/therapeutic use , Hepatic Artery/pathology , Liver Transplantation/methods , Thrombosis/prevention & control , Adult , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Cross-Sectional Studies , Female , Graft Survival , Hemostasis , Humans , Immunosuppressive Agents/therapeutic use , Liver Failure/surgery , Male , Middle Aged , Platelet Aggregation Inhibitors/therapeutic use , Treatment Outcome , Young AdultABSTRACT
Nontraumatic rhabdomyolysis in drug abusers is well-known, with cocaine and parenteral heroin the most frequent causative agents. Rhabdomyolysis is thought to result from compromised vascular supply to dependent muscles, due to prolonged pressure during long periods of depressed consciousness and immobility. However, recent work in rats has shown marked vasodilatation in areas of injured muscle, mediated by the nitric oxide pathway. Acute renal failure occurs in about 2/3 of the cases of cocaine-associated rhabdomyolysis. The usual clinical picture is that of a mentally obtunded drug addict presenting with swelling and tenderness of the muscles of a limb. However, these findings may be absent or overlooked. Characteristic laboratory features include elevated serum creatinine phosphokinase (CPK) (in excess of 90,000 IU/L) and myoglobinuria. We present a 33-year-old male addict who developed acute renal failure due to cocaine- and heroin-associated rhabdomyolysis. He had marked edema and tenderness of his right leg and was initially erroneously diagnosed as suffering from deep venous thrombosis. Only when the CPK was found to be 47,300 U/L, was the correct diagnosis made. Massive fluid replacement and alkalinization of the urine resulted in rapid improvement in renal function.
Subject(s)
Acute Kidney Injury/etiology , Cocaine , Rhabdomyolysis/complications , Substance-Related Disorders/complications , Acute Kidney Injury/diagnosis , Acute Kidney Injury/therapy , Adult , Animals , Diagnosis, Differential , Humans , Male , Rats , Rhabdomyolysis/diagnosis , Rhabdomyolysis/therapyABSTRACT
We describe the inhibitory effect of prostaglandins (PGs) on in vivo rat renal ammonia synthesis. The influence of systemic pH upon urinary PG excretion and ammoniagenesis was also investigated. Finally, PG production by incubated rat renal cortical slices was suppressed to investigate the PG-ammonia interplay in the absence of changes in renal blood flow, glomerular filtration rate, ambient electrolyte concentrations or extrarenal hormonal factors. In vivo ammonia synthesis doubled and PG excretion fell by 44% in normal rats, after intravenous administration of 1 mg/kg of meclofenamate. Higher doses of meclofenamate further augmented ammonia production and further reduced PG excretion. PG depletion was also associated with an increase in fractional excretion of ammonia (FENH3) that was independent of changes in urine flow rate or pH. Acute metabolic acidosis (AMA) increased total ammonia synthesis but also stimulated PG production. Administration of meclofenamate to rats with mild AMA markedly reduced urinary PG excretion, further augmented ammonia synthesis, and significantly increased the FENH3. Inhibition of stimulated PG synthesis during severe AMA did not increase ammoniagenesis or FENH3. Acute metabolic alkalosis did not alter production of PGs or ammonia, but reduced the FENH3 by 42%. Meclofenamate nearly normalized the FENH3 but stimulated synthesis to a lesser degree than was seen in nonalkalotic rats that received meclofenamate. Inhibition of PG synthesis in incubated rat renal cortical slices also stimulated ammoniagenesis. Conversely, stimulation of PG synthesis decreased ammonia production and acidification of the incubation medium increased prostaglandin F2 alpha production. Thus, in vitro findings support the in vivo results. We conclude that PGs inhibit ammonia synthesis in normal rats and in those undergoing mild AMA. Severe acidosis overrides this inhibitory effect of PGs, whereas metabolic alkalosis suppresses the stimulatory effect of PG synthesis inhibition.