Relationship between aerobic fitness and lower limb skin temperature during cycling exercise testing among well-trained athletes and nonathletes: a cross-sectional study.

Background: During prolonged physical exercise, the skin plays an important role in thermoregulation by dissipating heat to maintain core temperature. Moreover, thermal variation may be influenced by the physical fitness level of an individual. The aim of the present study was to determine the relationship between aerobic fitness and lower limb skin temperature during graded cycling exercise testing in well-trained athletes and nonathletes. Methods: Twelve trained athletes (mean ± SD maximal oxygen consumption [VO2max], 52.44 ± 4.5 ml/kg/min) and 12 nonathletes (VO2max, 36.95 ± 4.9 ml/kg/min) participated in this study. The regional skin temperature over the lower limbs was monitored continuously during incremental exercise testing using a thermal camera, and cardio-respiratory parameters were assessed and recorded using a metabolic analyzer (K5, COSMED, Rome, Italy). Results: The mean skin temperature of athletes at a high intensity of exercise was 27.23 ± 0.3 °C while that of nonathletes was 29.03 ± 0.44 °C, a difference that was statistically significant (p < 0.05). A negative correlation was observed between skin temperature and cardiovascular parameters (VO2max and heart rate) in athletes, while no such correlation was found among nonathletes. Conclusion: The present study demonstrated a negative correlation between oxygen consumption and lower limb skin temperature in athletes, while the correlation was poor in nonathletes. This suggests that physical fitness level may influence the pattern of alterations in lower limb skin temperature, which supports the hypothesis that athletes exhibit better heat dissipation mechanisms than nonathletes.

Simplifying biometry in oil-filled eyes: A novel formula for axial length calculation in eyes with 1000 cSt silicone oil.

Purpose: To derive a formula for accurate axial length (AL) assessment using routine ultrasound in silicone oil-filled eyes, where optical biometry is unavailable or not possible. Methods: This was a prospective, consecutive, nonrandomized study of 50 eyes of 50 patients conducted in a tertiary care hospital in North India. AL measurements were taken using both manual A-scan and IOL master, both in silicone oil-filled status and 3 weeks after silicone oil removal. A correction factor of 0.7 was used for AL adjustment in oil-filled eyes. The corrected AL (cAL) was compared with IOL master values in oil-filled eyes. Agreement analysis was carried out using Bland Altman plot. Linear regression analysis was done using uncorrected manual AL to find a new equation. Data was analyzed using Stata 14. A P value <0.05 was taken as significant. Results: The study included 40 males and 10 females, with an age range of 6-83 years (mean 41.9 years). The mean AL of the oil-filled eye as measured by manual A-scan was 31.76 mm ± 3.09 and by IOL master was 24.7 mm ± 1.74. Linear regression analysis was performed in randomly selected 35 eyes of the observed data to obtain a new equation: predicted AL (PAL) = 14 + 0.3 × manual AL. The mean difference between PAL and optically measured AL with silicone oil in situ was 0.98 ± 1.67. Conclusion: We propose a new formula for better prediction of the correct AL in silicone oil-filled eyes using ultrasound-based AL measurement.

Sharing and Teaching Electrocardiograms to Minimize Infarction (STEMI): reducing diagnostic time for acute coronary occlusion in the emergency department.

BACKGROUND: Limits to ST-Elevation Myocardial Infarction (STEMI) criteria may lead to prolonged diagnostic time for acute coronary occlusion. We aimed to reduce ECG-to-Activation (ETA) time through audit and feedback on STEMI-equivalents and subtle occlusions, without increasing Code STEMIs without culprit lesions. METHODS: This multi-centre, quality improvement initiative reviewed all Code STEMI patients from the emergency department (ED) over a one-year baseline and one-year intervention period. We measured ETA time, from the first ED ECG to the time a Code STEMI was activated. Our intervention strategy involved a grand rounds presentation and an internal website presenting weekly local challenging cases, along with literature on STEMI-equivalents and subtle occlusions. Our outcome measure was ETA time for culprit lesions, our process measure was website views/visits, and our balancing measure was the percentage of Code STEMIs without culprit lesions. RESULTS: There were 51 culprit lesions in the baseline period, and 64 in the intervention period. Median ETA declined from 28.0 min (95% confidence interval [CI] 15.0-45.0) to 8.0 min (95%CI 6.0-15.0). The website garnered 70.4 views/week and 27.7 visitors/week in a group of 80 physicians. There was no change in percentage of Code STEMIs without culprit lesions: 28.2% (95%CI 17.8-38.6) to 20.0% (95%CI 11.2-28.8%). Conclusions Our novel weekly web-based feedback to all emergency physicians was associated with a reduction in ETA time by 20 min, without increasing Code STEMIs without culprit lesions. Local ECG audit and feedback, guided by ETA as a quality metric for acute coronary occlusion, could be replicated in other settings to improve care.

Using ECG-To-Activation Time to Assess Emergency Physicians' Diagnostic Time for Acute Coronary Occlusion.

BACKGROUND: There is no quality metric for emergency physicians' diagnostic time for acute coronary occlusion. OBJECTIVE: We sought to quantify diagnostic time associated with automated interpretation, classic ST-elevation myocardial infarction (STEMI) criteria, STEMI-equivalents, and subtle occlusions, using electrocardiogram (ECG)-to-activation of catheterization laboratory time. METHODS: This multicenter retrospective study reviewed all code STEMI patients from the emergency department (ED) with confirmed culprit lesions from January 2016 to December 2018. We measured door-to-ECG (DTE) time and ECG-to-activation (ETA) time. We examined the first ED ECGs to determine whether automated interpretation labeled "STEMI," and they met classic STEMI criteria, STEMI-equivalents, or rules for subtle occlusion. ECG analysis was performed by two emergency physicians blinded to clinical scenario, automated interpretation, and angiographic outcome. RESULTS: There were 177 code STEMIs with culprit lesions, with a median DTE time of 9.0 min and a median ETA time of 16.0 min. Automated interpretation labeled 55.4% of first ECGs "STEMI" (ETA 6.5 min) and 44.6% not "STEMI" (ETA 66 min, p < 0.0001). Of first ECGs, 63.8% met classic STEMI criteria (ETA 8.0 min), 8.5% had STEMI-equivalents (ETA 32.0 min, p = 0.0026), 16.4% had subtle occlusions (ETA 89.0 min, p = 0.045), and 11.3% had no diagnostic sign of occlusion (ETA 68.0 min, p = 0.20). CONCLUSIONS: STEMI criteria missed more than one-third of occlusions on first ECG, but most had STEMI-equivalents or rules for subtle occlusion. ETA time can serve as a quality metric for emergency physicians to promote new ECG insights and assess quality improvement initiatives.

Metastatic subretinal abscess in a patient with perinephric abscess.

An 80-year-old lady with uncontrolled type 2 diabetes developed fever and abdominal pain followed by a sudden diminution of vision in her left eye. Right infra-renal abscess accounted for abdominal pain. A metastatic left subretinal abscess was diagnosed subsequently. Medical management for her systemic condition initiated. Vitreous biopsy was performed along-with intravitreal antibiotic administration. Because of no clinical recovery, patient underwent pars plana vitrectomy. Prompt systemic stabilization and a timely surgical intervention in the left eye resulted in a satisfactory visual gain. Metastatic subretinal abscess following a perinephric abscess is rare phenomenon and only a few cases are reported to date.

Temporal changes in physiological and molecular markers in various brain regions following transient global ischemia in rats.

Several mechanisms are involved in the loss of cellular integrity and tissue destructions in various brain regions during ischemic insult. The affected brain employs various self-repair mechanisms during the poststroke recovery. Therefore, the current study involves time course changes in different brain regions following ischemia in terms of inflammation, oxidative stress and apoptosis for which a bilateral common carotid arteries occlusion model was chosen. The development of oxidative stress was seen with a marked increase in ROS and NO levels with concomitant decrease in GSH levels and also the activities of anti-oxidant enzymes. These alterations were accompanied with decreased levels of neurotransmitters and motor and cognitive deficits at various time points. Increased expressions of various pro-inflammatory cytokines and a decline in BDNF levels in hippocampal regions on 7th day post ischemia, suggesting their role in its pathogenesis. The restoration of BDNF and neurotransmitter levels along with significant decline in inflammatory cytokine levels 14th day onwards following ischemia in hippocampus suggested poststroke recovery. The extent of neuronal damage was found to be increased significantly on 7th day post ischemia as indicated by TUNEL assay and hematoxylin and eosin staining depicting enhanced number of pyknotic neurons in cortical and hippocampal regions. Cortical regions of the ischemic brains were severely affected while hippocampal regions showed significant poststroke recovery, which might attributed to the normalization of BDNF and pro-inflammatory cytokine levels. In conclusion, the present study established the central role of BDNF and pro-inflammatory cytokines in the poststroke recovery. Also, the cortical and hippocampal regions were found to be more susceptible for ischemic injury. As our results indicated, full recovery after ischemic injury in different brain regions was not achieved, therefore further studies with long-term recovery time are required to be conducted.

Sympathetic Ophthalmia: Experience from a Tertiary Care Center in Northern India.

PURPOSE: To describe our clinical experience with sympathetic ophthalmia (SO) at a tertiary eye care center in north India. METHODS: In this retrospective case series, analysis of the clinical features and visual outcomes of patients diagnosed with SO between March 2012 and March 2016 were performed. RESULTS: Ten male and four female patients (median age, 15.5 years) with SO following penetrating trauma (10 patients) or ocular surgery (four patients) were included. SO developed 2 weeks to 3 years after the insult. Mean presenting visual acuity of the sympathizing eyes was 1.086 (LogMAR). Anterior chamber reaction was documented in all eyes in which it could be assessed (14 sympathizing eyes; five exciting eyes). Neurosensory detachment was seen in 10 of 14 patients (71.5%). Five patients (35.7%) were managed with oral steroids alone, whereas nine (64.3%) were treated with intravenous pulse dexamethasone followed by oral steroids. Inflammation recurred in three patients during steroid tapering, necessitating restarting of steroid therapy with or without additional immunosuppressants. At the last follow-up, all 14 patients were in remission with low-dose oral steroids; seven patients were also on immunosuppressants. At the final follow-up, 12 of 14 (85.7%) sympathizing eyes achieved 20/40 or better visual acuity and three exciting eyes achieved at least 6/24 visual acuity. CONCLUSION: Although SO is a potentially blinding disorder, early detection and individualized treatment allow most patients achieve good final visual acuity.

Effect of the NADPH oxidase inhibitor apocynin on ischemia-reperfusion hippocampus injury in rat brain.

Blockage along with sudden restoration of blood following ischemia, results in several cascading events, such as a massive ROS production which plays an important role in the pathophysiology of ischemia. NADPH oxidase complex in mitochondria complex is believed to be the major source for ROS production. The present study explores the therapeutic potential of apocynin, an NADPH oxidase inhibitor in attenuating the ROS production, and the resultant neuroinflammation and mitochondrial injury during cerebral ischemia in rats. Bilateral common carotid artery occlusion (BCCAO) model was chosen for the study where intracellular ROS and NO levels as well as the NADPH oxidase activity were found to be increased significantly post 7th day of ischemic injury. Enhanced glial activation was observed and an upregulated expression of GFAP and Iba-1 in hippocampus along with that of the transcription factor NFκB and inflammatory markers iNOS, IL-1α, IL-1ß and TNF-α.The activity of mitochondrial electron transport chain (ETC) complexes I, II, IV and V were significantly decreased following ischemia. Consequently, there was a decrease in mitochondrial membrane potential (MMP) while an increased release of cytochrome c and upregulated apoptotic markers Bax, caspase-3 and 9 initiated the programmed neuronal death which was also reflected by the marked increase in TUNEL positive cells in the hippocampal region. The physiological functional alterations have been observed following ischemic injury i.e memory and motor deficits. The apocynin supplementation significantly reduced the NADPH oxidase activity and resulted in declined ROS production which in-turn prevented the glial activation and downregulated the inflammatory and pro-apoptotic markers. Apocynin also restored the MMP (Δψm) and mitochondrial enzymes via inhibition of ROS vicious and relationship between NADPH oxidase and mitochondrial complexes. Apocynin treatment was also successfully reduced the behavioural deficits in ischemic animals. In conclusion, inhibiting the NADPH oxidase complex presumably attenuated the mitochondrial injury, neuroinflammation and apoptosis following ischemic injury in rat brain.

Alzheimer's disease like pathology induced six weeks after aggregated amyloid-beta injection in rats: increased oxidative stress and impaired long-term memory with anxiety-like behavior.

OBJECTIVES: Amyloid-beta (Aß) peptide deposition into insoluble plaques is a pathological hallmark of Alzheimer's disease (AD), but soluble oligomeric Aß is considered to be more potent and has been hypothesized to directly impair learning and memory. Also, evidences from some clinical studies indicated that Aß oligomer formation is the major cause for early AD onset. However, the biochemical mechanism involved in the oligomer-induced toxicity is not very well addressed. So, thise present study was undertaken to study the effects of single intracerebroventricular (icv) injection of protofibrillar Aß 1-42 on the behavioral and biochemical profile in rats. METHODS: Rats were divided into two groups (n = 8 per group): (1) sham control group and (2) Aß 1-42 injected group. A single dose of protofibrillar Aß 1-42 (5 ul) through icv injection was bilaterally administered into the dorsal hippocampus, while sham control animals were administered with 5 µl of vehicle. RESULTS: The results demonstrated that the protofibrillar Aß significantly inhibited long-term memory retention and increased anxiety levels as shown by the behavioral studies. The amyloid deposits were present inside the brain even six weeks after injection as confirmed by thioflavin-T staining and the neurodegeneration induced by these deposits was confirmed by Nissl's staining in hippocampal and cortical regions. The amyloid aggregates induced reactive oxygen species (ROS) production, acetylcholinesterase activity, nitrite levels, lipid peroxidation, and inhibited antioxidant enzyme activity in hippocampus, cortex, and striatum regions of rat brain after six weeks. DISCUSSION: The present study indicated that protofibrillar Aß 1-42 injection altered long term memory, induced anxiety-like behavior and also developed Alzheimer's disease like pathology in rats.

Apocyanin, NADPH oxidase inhibitor prevents lipopolysaccharide induced α-synuclein aggregation and ameliorates motor function deficits in rats: Possible role of biochemical and inflammatory alterations.

Parkinson's disease (PD), is an age-related, progressive neurodegenerative disorder that affects movement and is characterized by the loss of dopaminergic neurons in the nigrostriatal region. Although the clinical and pathological features of PD are complex, recent studies have indicated that microglial NADPH oxidase play a key role in its pathology. A little information is available regarding the role of apocyanin, an NADPH oxidase inhibitor, in ameliorating α-synuclein aggregation and neurobehavioral consequences of PD. Therefore, the present study evaluated its therapeutic potentials for the treatment of neurobehavioral consequences in lipolysaccharide (LPS) induced PD model. For the establishment of PD model LPS (5 µg/5 µl PBS) was injected into the Substantia nigra (SN) of rats. Apocyanin (10mg/kgb.wt) was injected intraperitoneal. Statistical analysis revealed that apocynin significantly ameliorated LPS induced inflammatory response characterized by NFkB, TNF-α and IL-1ß upregulation as assessed by ELISA. It also prevented dopaminergic neurons from toxic insult of LPS as indicated by inhibition of apoptotic markers i.e., caspase 3 and caspase 9 as depicted from RT-PCR and ELISA studies. This was further supported by TUNEL assay for DNA fragmentation. Effectiveness of apocyanin in protecting dopaminergic neuronal degeneration was further confirmed by assessment of α-synuclein deposition as depicted by IHC analysis. Consequently, an improvement in the behavioral outcome was observed following apocyanin treatment as depicted from various behavioral tests performed. Hence the data suggests that specific NADPH oxidase inhibitors, such as apocynin, may provide a new therapeutic approach to the control of neurological disabilities induced by LPS induced PD.