Acute Biochemical Changes Research Articles

Immediate Biochemical Changes After Gait Biofeedback in Individuals With Anterior Cruciate Ligament Reconstruction.

Gait biomechanics are linked to biochemical changes that contribute to the development of posttraumatic knee osteoarthritis in individuals with anterior cruciate ligament reconstruction (ACLR). It remains unknown if modifying peak loading during gait using real-time biofeedback will result in acute biochemical changes related to cartilage metabolism. To determine if acutely manipulating peak vertical ground reaction force (vGRF) during gait influences acute changes in serum cartilage oligomeric matrix protein concentration (sCOMP) among individuals with ACLR. Crossover study. Thirty individuals with unilateral ACLR participated (70% female, age = 20.43 ± 2.91 years old, body mass index = 24.42 ± 4.25, months post-ACLR = 47.83 ± 26.97). Additionally, we identified a subgroup of participants who demonstrated an increase in sCOMP after the control or natural loading condition (sCOMPCHANGE > 0 ng/mL, n = 22, 70% female, age = 20.32 ± 3.00 years old, body mass index = 24.73 ± 4.33, months post-ACLR = 47.27 ± 29.32). Serum was collected both prior to and immediately after each condition to determine sCOMPchange. All participants attended 4 sessions that involved 20 minutes of walking on a force-measuring treadmill consisting of a control condition (natural loading) followed by random ordering of 3 loading conditions with real-time biofeedback: (1) symmetric vGRF between limbs, (2) a 5% increase in vGRF (high loading) and (3) a 5% decrease in vGRF (low loading). A general linear mixed model was used to determine differences in sCOMPCHANGE between altered loading conditions and the control group in the entire cohort and the subgroup. The sCOMPCHANGE was not different across loading conditions for the entire cohort (F3,29 = 1.34, P = .282). Within the subgroup, sCOMPCHANGE was less during high loading (1.95 ± 24.22 ng/mL, t21 = -3.53, P = .005) and symmetric loading (9.93 ± 21.45 ng/mL, t21 = -2.86, P = .025) compared with the control condition (25.79 ± 21.40 ng/mL). Increasing peak vGRF during gait decreased sCOMP in individuals with ACLR who naturally demonstrated an increase in sCOMP after 20 minutes of walking. ClinicalTrials.gov (NCT03035994).

Detection of the Incidence of Infections and Acute Biochemical Changes in Diffused Large B-Cell Lymphoma Patients Treated with Cyclophosphamide, Doxorubicin, Vincristine and Prednisone (CHOP) with and without Rituximab

Acute biochemical changes, hepatotoxicity, nephrotoxicity and frequency of infections are common in diffuse large B-cell Lymphoma patients undergoing Cyclophosphamide, Doxorubicin, Oncovin (Vincristine) Prednisone (CHOP) and Rituximab plus CHOP chemo cycles. Eventually, it leads to prolonging hospital stay and suspending the next chemotherapy cycles. The objectives of our study were to determine the changes in biochemical disturbances induced by CHOP or RCHOP and second objective was to compare the effect of CHOP with or without rituximab on the incidence of the infections such as (Cytomegalovirus, Herpes Simplex Virus and Varicella-Zoster virus), bacterial infections and tuberculosis. Files were prospectively reviewed during the tenure of 2014-2016. Participants aged greater than or equal to 18 years old with a known case of DLBCL undergoing CHOP or RCHOP chemotherapy were allowed to be included in the study. Baseline and posttreatment patients profile of blood chemistry, liver functions test was collected and compared with the Common Terminology Criteria for adverse events v3.0 2009 CTCAE 2009 and the data regarding infection of Cytomegalovirus, Herpes Simplex Virus and Vericella-Zoster virus, bacterial infections and tuberculosis were drawn from the participant's profile. Patients treated with CHOP therapy showed a significant difference of Alkaline Phosphatase (ALP) (p-value 0.009), direct bilirubin (p-value 0.034) and serum glutamic-pyruvic transaminase (SGPT) (p-value 0.004). Bacterial Pneumonia was only 1 (5%) and 1 (5%) CMV reported positive after the R-CHOP. We propose that liver profile including (bilirubin, SGOT and SGPT) Urea, Creatinine and electrolytes should strictly be considered if found deranged before every treatment cycle and suspend chemotherapy in case of moderate or severe toxicity.

Fixing Hearts and Protecting Minds

Ischemic heart disease is a significant cause of mortality and morbidity in Western populations. Consistent with this, coronary artery bypass graft (CABG) surgery remains one of the most frequently performed major surgeries. Improved survival rates mean that our research focus now extends beyond surgical technique to include quality of postoperative outcome. Postoperative cognitive dysfunction (POCD) has emerged as one of the most challenging and hotly debated issues, with increasing impetus to answer the unresolved question: does fixing the heart come at a cost to the brain? CABG surgery is associated with neurological events including stroke in 1.6%1 and delirium in 5.8%2 of patients. Beyond these severe and marked alterations to neurological function, there has been a widely held belief that CABG surgery is associated with POCD, which may presage a decline toward dementia. Research has been influenced by the 1995 Consensus Statement3 into the study of POCD in patients undergoing CABG surgery. Although the methods of investigation set forth by the Consensus Statement achieved widespread acknowledgment, its specific recommendations have not always been followed.4 Despite significant methodological issues, it seems that the balance of interpretation has historically been in favor of CABG surgery as a cause of significant POCD. More recently, however, a review of a series of publications from a well-controlled longitudinal cohort study conducted at Johns Hopkins5 and a meta-analysis6 suggested that cognition is in fact stable or may even show some improvement after CABG surgery in the majority of patients, at least within the first year (Figures 1 and 2). There is little doubt that POCD affects some patients in the short term, but the pathophysiological mechanisms underlying this and the influence on longer-term cognitive function remain uncertain. For research to progress, we require a paradigmatic shift in our focus from …

Acute effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on dopamine metabolism in mouse and rat striatum

Monoamines and metabolites in mouse striatum were measured at intervals (0-6 h) after injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 50 mg kg-1 subcutaneously). In addition, the accumulation of 3,4-dihydroxyphenylalanine (dopa), induced by inhibition of the aromatic amino acid decarboxylase by 3-hydroxybenzylhydrazine (NSD 1015), was assessed during every 15 min (0-135 min) after MPTP administration. The alterations induced by MPTP during the first hour after injection were a transient acceleration followed by a marked retardation of dopa synthesis, a decrease in 3,4-dihydroxyphenylacetic acid (DOPAC; -55%) and an increase in 3-methoxytyramine (3-MT; +400%). Between 60 and 75 min after administration, some dramatic changes took place: a 40% reduction of dopamine (DA), a marked additional increase in 3-MT (to 1300% of control) and an increase in homovanillic acid (HVA; +50%). The period after 75 min was characterized by a further depletion of DA, a decrease in 3-MT and a transient increase in HVA (max. 240% of control). Six hours after the administration, all concentrations of DA and its metabolites were subnormal, i.e. DA (30% of control), 3-MT (10%), DOPAC (10%) and HVA (65%). The MPTP-induced retardation of dopa synthesis was not antagonized by haloperidol or by reserpine pretreatment. MPTP (25 or 50 mg kg-1 s.c.) produced similar acute changes in the levels of DA and its metabolites in rat as in mouse striatum, though much less pronounced.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed neuropathology after carbon monoxide poisoning is immune-mediated.

The neuropathological sequelae of carbon monoxide (CO) poisoning cannot be explained by hypoxic stress alone. CO poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes. Lymphocytes from CO-poisoned rats subsequently exhibit an auto-reactive proliferative response to MBP, and there is a significant increase in the number of activated microglia in brain. Rats rendered immunologically tolerant to MBP before CO poisoning exhibit acute biochemical changes in MBP but no lymphocyte proliferative response or brain microglial activation. CO poisoning causes a decrement in learning that is not observed in immunologically tolerant rats. These results demonstrate that delayed CO-mediated neuropathology is linked to an adaptive immunological response to chemically modified MBP.

Acute Biochemical Responses of a Submersed Macrophyte, Potamogeton crispus L., to High Ammonium in an Aquarium Experiment

ABSTRACT Acute biochemical responses of Potamogeton crispus L. to high external ammonium were investigated in an aquarium experiment. Shoots of P: crispus were incubated in aquaria for 24 h or 48 h at five treatments of ammonium-0, 1, 5, 10 and 20 mg/L NH4-N. Soluble sugar content of the shoots declined markedly with increasing ammonium levels, whereas soluble amino acid content increased dramatically. Responses of two antioxidant enzymes as well as soluble protein content fit a lognormal distribution with increasing ammonium levels. High ammonium levels (NH4-N≥5 mg/L) caused significant acute biochemical changes in P. crispus, which potentially could lead to significant biochemical damage.

Ipsilateral and contralateral testicular biochemical acute changes after unilateral testicular torsion and detorsion

Objectives An experimental study has been conducted to investigate testicular blood flow alterations through acute biochemical changes during unilateral testicular torsion and detorsion. Methods One hundred twenty male albino rats were divided into 12 groups, each containing 10 rats. One group served to determine basal values of biochemical parameters, 4 groups were subjected to varying periods of unilateral testicular torsion (3, 6, 12, and 24 hours, respectively), 3 groups were subjected to detorsion following varying periods of torsion (6, 12, and 24 hours, respectively), and 4 groups underwent sham operations as controls. Levels of lactic acid, hypoxanthine, and lipid peroxidation products were determined in testicular tissues. Results Values of these 3 parameters obtained from sham operation control groups didnot differ significantly from basal values (p > 0.05). All 3 parameters were increased significantly in both ipsilateral torted and contralateral nontorted testes after unilateral testicular torsion when compared with basal values (p < 0.05). Detorsion did not cause significant changes in levels of lipid peroxidation products in both ipsilateral torted and contralateral nontorted testes when compared with values obtained after torsion (p > 0.05). Conclusions Ipsilateral testicular torsion causes a decrease not only in the ipsilateraltorted but also in the contralateral nontorted testicular perfusion. The clues of reperfusion injury do not become evident following detorsion of testicular torsion lasting more than 6 hours.

Effects of glutamate, quisqualate, and N-methyl- d-aspartate in neonatal brain

The intracerebral injection of the excitotoxins, glutamate (GLU), or its analogues, quisqualic acid (QA) and N-methyl- d-aspartate (NMDA), produces neuropathologic changes which resemble those induced by hypoxic-ischemic injury. We employed proton magnetic resonance spectroscopy to investigate the acute biochemical changes which follow injection of these excitotoxins in the neonatal rat brain. Aspartate and GLU increased in animals injected with GLU or NMDA. Alanine, glycine, and taurine increased with all three excitotoxins. There was no decrease in phosphocreatine (PCr) or glucose and only a modest increase in lactate after excitotoxin injection, but there was substantial change in these metabolites after hypoxia. GABA rose only after hypoxic-ischemic injury. Although NMDA and QA produced morphological changes which resembled those following hypoxic-ischemic injury, the effect of these excitotoxins on levels of PCr, glucose, and excitatory and inhibitory amino acids was considerably different.

Biochemical changes in the rat lung and liver following intratracheal instillation of cadmium oxide

Acute biochemical changes in the rat lung and liver following intratracheal instillation of cadmium oxide (CdO) were observed at a dose of 5 μ Cd/rat to investigate the defense mechanism to Cd intoxication via airway. In the lung metallothionein (MT) was induced, reaching a maximum at 2 days. A slight increase in reduced glutathione (GSH) concentration was observed at 4 days. The activity of glucose-6-phosphate dehydrogenase (G6PDH) was increased and Superoxide dismutase (SOD) activity was slightly decreased, but glutathione peroxidase (GPx) and glutathione reductase (GR) activities were not changed. These observations suggested that MT played a key role in detoxification of instilled CdO, but that the antioxidant enzymes had a minimal role. In the liver MT and GSH concentrations were diminished 7 h after instillation and returned to their control levels. Hepatic GPx activity was increased 1 day after instillation and the significantly elevated level lasted up to 7 days, while hepatic GR activity was decreased. These hepatic biochemical changes are suggested to be due to the secondary effects of the lung injury.

Acute effects of 1-methyl-4-phenylpyridinium ion (MPP+) on dopamine and serotonin metabolism in rat striatum as assayed in vivo by a micro-dialysis technique.

The acute effect of 1-methyl-4-phenylpyridinium ion (MPP+), a neurotoxin derived from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), was examined by the in vivo micro-dialysis technique. A dialysis cannula was implanted into rat striatum, and the changes in the concentrations of dopamine (DA), 3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) in the perfusate every 20 min after administration of MPP+ were determined by high-performance liquid chromatography with electrochemical detection (HPLC-ED). After MPP+ administration the levels of DOPAC, HVA and 5-HIAA were markedly decreased. On the contrary the level of DA was markedly increased and reached a maximum 40 min after beginning of the MPP+ administration. By postmortem analysis of the striatal tissue MPP+ was proved to cause the inhibition of monoamine oxidase (MAO), especially MAO-B. These results suggest that the acute biochemical changes induced by MPP+ in vivo were MAO inhibition and release of DA.

Acute biochemical changes in rat liver induced by the naturally occurring amino acid indospicine

Preliminary observations have been made on the hepatotoxicity to female rats of indospicine (L-2-amino-6-amidino hexanoic acid) the toxic principle of the seed of Indigofera spicata Forsk, previously shown to be hepatotoxic to mice. A dose of 2 g kg given by stomach tube produced a marked rise in the levels of liver triglycerides which reached a maximum at 24 hr and thereafter declined. Progressive enlargement of the liver occurred and continued even when, at 40 hr, liver lipid levels were falling. Although small increases in the liver content of protein, DNA and RNA were found, about 75 per cent of the increment in liver weight was due to water. The increase in water content was paralleled by an increase in cations, though the relative proportions of the cations to each other were unchanged. Liver ATP levels were not decreased. A significant inhibition of incorporation of leucine-1- 14C into liver and serum protein was observed at 5, 12, and 24 hr after treatment. At 40 hr incorporation was enhanced. The inhibition of protein synthesis preceded the rise in liver lipid.