Impact of Delayed Pain to Needle and Variable Door to Needle Time On In-Hospital Complications in Patients With ST-Elevation Myocardial Infarction Who Underwent Thrombolysis: A Single-Center Experience.

Background Myocardial infarction is a life-threatening event, and timely intervention is essential to improve patient outcomes and mortality. Previous studies have shown that the time to thrombolysis should be less than 30 minutes of the patient\u27s arrival at the emergency room. Pain-to-needle time is a time from onset of chest pain to the initiation of thrombolysis, and door-to-needle time is a time between arrival to the emergency room to initiation of thrombolytic treatment. Ideally, the target for door-to-needle time should be less than 30 minutes; however, it is unclear if the door-to-needle time has a significant impact on patients presenting later than three hours from the onset of pain. As many of the previous studies were conducted in first-world countries, with established emergency medical services (EMS) systems and pre-hospital ST-elevation myocardial infarction (STEMI) triages and protocols, the data is not completely generalizable to developing countries. We, therefore, looked for the impact of the shorter and longer door-to-needle times on patient outcomes who presented to the emergency room (ER) with delayed pain-to-needle times (more than three hours of pain onset). Objective To determine the impact of delayed pain-to-needle time (PNT) with variable door-to-needle time (DNT) on in-hospital complications (post-infarct angina, heart failure, left ventricular dysfunction, and death) in patients with ST-elevation myocardial infarction (STEMI) who underwent thrombolysis. Methods and results A total of 300 STEMI patients who underwent thrombolysis within 12 hours of symptoms onset were included, which were divided into two groups based on PNT. These groups were further divided into subgroups based on DNT. The primary outcome was in-hospital complications between the two groups and between subgroups within each group. The pain-to-needle time was ≤3 hours in 73 (24.3%) patients and \u3e3 hours in 227 (75.7%) patients. In-hospital complications were higher in group II with PNT \u3e3 hours (p3 hours), has a significant impact on in-hospital complications with no difference in mortality

GABA ergic transmission in rat pontine reticular formation regulates the induction phase of anesthesia and modulates hyperalgesia caused by sleep deprivation

The oral part of the pontine reticular formation (PnO) contributes to the regulation of sleep, anesthesia and pain. The role of PnO γ‐aminobutyric acid ( GABA ) in modulating these states remains incompletely understood. The present study used time to loss and time to resumption of righting response (Lo RR and Ro RR ) as surrogate measures of loss and resumption of consciousness. This study tested three hypotheses: (i) pharmacologically manipulating GABA levels in rat PnO alters Lo RR , Ro RR and nociception; (ii) propofol decreases GABA levels in the PnO; and (iii) inhibiting GABA synthesis in the PnO blocks hyperalgesia caused by sleep deprivation. Administering a GABA synthesis inhibitor [3‐mercaptopropionic acid (3‐ MPA )] or a GABA uptake inhibitor [nipecotic acid ( NPA )] into rat PnO significantly altered Lo RR caused by propofol. 3‐ MPA significantly decreased Lo RR for propofol (−18%). NPA significantly increased Lo RR during administration of propofol (36%). Neither 3‐ MPA nor NPA altered Ro RR following cessation of propofol or isoflurane delivery. The finding that Lo RR was decreased by 3‐ MPA and increased by NPA is consistent with measures showing that extracellular GABA levels in the PnO were decreased (41%) by propofol. Thermal nociception was significantly decreased by 3‐ MPA and increased by NPA , and 3‐ MPA blocked the hyperalgesia caused by sleep deprivation. The results demonstrate that GABA levels in the PnO regulate the time for loss of consciousness caused by propofol, extend the concept that anesthetic induction and emergence are not inverse processes, and suggest that GABA ergic transmission in the PnO mediates hyperalgesia caused by sleep loss. The intravenous anesthetic propofol significantly decreases extracellular GABA levels in rat PnO. Pharmacologically increasing or decreasing extracellular GABA levels increases or decreases, respectively, the time to loss of consciousness caused by propofol. GABAergic transmission in the PnO does not modulate the resumption of consciousness after isoflurane‐ and propofol‐anesthesia. Administration of a GABA synthesis inhibitor into the PnO blocks the hyperalgesia caused by sleep deprivation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/108018/1/ejn12571.pd

Tactile sensory and pain networks in the human spinal cord and brain stem mapped by means of functional MR imaging.

Background and purposeTouch and brush sensory stimuli elicit activity in discriminative touch pathways involving specific regions in the spinal cord and brain stem. However, no study has mapped normal sensory activity noninvasively in healthy humans. The purpose of this study is to map the neuronal activity of sensory input to understand abnormal sensory transmission.Materials and methodsIn the present study, spinal fMRI (by using SEEP) was used to map the activity involved with light touch (2 g and 15 g von Frey filaments) and brush stimuli in the brain stem and spinal cords of 8 healthy volunteers. The results were spatially normalized and analyzed with custom-made software. Areas of SEEP activity were identified by using general linear model analysis.ResultsThe 2 g von Frey filament showed predominant activity in the medulla around the ipsilateral dorsal gracile and cuneate nuclei. The 15 g filament elicited significant activity in the ipsilateral dorsal and contralateral ventral gray matter areas of the spinal cord, areas around the olivary nuclei, pontine reticular formation, periaqueductal gray, and raphe nuclei in the rostral pons and midbrain. The brush stimuli elicited more activity in the medulla around the ipsilateral cuneate and gracile nuclei.ConclusionsThe 2 g filament and brush stimuli activated areas associated with a touch response. The 15 g filament activated areas associated with a pain response. The results from this study identify specific neuronal regions in the brain stem and spinal cord involved in sensory transmission and help understand altered sensory and pain states

Tactile sensory and pain networks in the human spinal cord and brain stem mapped by means of functional MR imaging.

Background and purposeTouch and brush sensory stimuli elicit activity in discriminative touch pathways involving specific regions in the spinal cord and brain stem. However, no study has mapped normal sensory activity noninvasively in healthy humans. The purpose of this study is to map the neuronal activity of sensory input to understand abnormal sensory transmission.Materials and methodsIn the present study, spinal fMRI (by using SEEP) was used to map the activity involved with light touch (2 g and 15 g von Frey filaments) and brush stimuli in the brain stem and spinal cords of 8 healthy volunteers. The results were spatially normalized and analyzed with custom-made software. Areas of SEEP activity were identified by using general linear model analysis.ResultsThe 2 g von Frey filament showed predominant activity in the medulla around the ipsilateral dorsal gracile and cuneate nuclei. The 15 g filament elicited significant activity in the ipsilateral dorsal and contralateral ventral gray matter areas of the spinal cord, areas around the olivary nuclei, pontine reticular formation, periaqueductal gray, and raphe nuclei in the rostral pons and midbrain. The brush stimuli elicited more activity in the medulla around the ipsilateral cuneate and gracile nuclei.ConclusionsThe 2 g filament and brush stimuli activated areas associated with a touch response. The 15 g filament activated areas associated with a pain response. The results from this study identify specific neuronal regions in the brain stem and spinal cord involved in sensory transmission and help understand altered sensory and pain states

TECHNO-ECONOMIC ANALYSIS OF PHOTOCATALYSIS UNDER LIGHT IRRADIATION USING TIO2, WO3, AND WO3/CQDS IN REMOVAL OF METHYLENE BLUE DYE

Due to the enormous production of coloured effluent polluted with dyes and other chemical auxiliaries, the textile industry is one of the most environmentally unfriendly industrial processes

Spontaneous Bacterial Peritonitis and Anasarca in a Female Patient with Ovarian Hyperstimulation Syndrome Complicated by Respiratory and Kidney Failure

Ovarian hyperstimulation syndrome (OHSS) was first described in 1960. It may occur as a complication of gonadotropin hormone therapy during assisted pregnancy or for primary infertility. A 26-year-old female patient with polycystic ovarian syndrome and primary infertility was treated to conceive. She received intravenous gonadotropin-releasing hormone (GnRH) along with follicle-stimulating hormone in an outside private clinic. She presented to the emergency department with abdominal and chest pain, loose stool, vomiting, shortness of breath and decreasing urine output. She was found to have edema, ascites, effusion and acute kidney injury (AKI). Considering the symptoms preceding the drug history and anasarca, a diagnosis of severe OHSS was made. Ascites was further complicated by spontaneous bacterial peritonitis (SBP), which had already been reported before. We speculate that low immunity due to decreased immunoglobulin in patients with OHSS makes them prone to SBP. In our case, septicemia secondary to SBP and fluid loss due to capillary leakage from OHSS resulted in AKI and respiratory failure. This critically ill patient was treated in a special care unit, and she fully recovered with supportive measures. Severe OHSS may present as anasarca including ascites which can develop SBP leading to sepsis and multiorgan failure