Evaluation of Peripheral Nerves In Patients Receiving Anti -Tnf- α Drug Therapy

Objective. This study aims to evaluate the efficacy of moxibustion on joint swelling and pain and the levels of C-X-C motif chemokine ligand 1 (CXCL1), β-endorphin (β-EP) in serum of rheumatoid arthritis (RA) patients and to investigate the anti-inflammatory and analgesic mechanism of moxibustion on improving RA. Methods. Sixty-eight patients with RA were randomly and equally classified into the control and treatment groups. The control group was treated with routine drug therapy, while the treatment group received routine drug therapy and moxibustion. Both groups were treated for eight weeks. The symptoms and laboratory indicators of RA patients were compared in the two groups before and after intervention. Results. Sixty-one patients completed the study: four patients dropped out from the treatment group and three from the control group. Trial endpoints were change (∆) in symptoms, measured by Ritchie’s articular index (RAI), swollen joint count (SJC), and laboratory indicators, measured by the level of CXCL1, β-EP, tumor necrosis factor-a (TNF-α), and interleukin-1β (IL-1β). ∆RAI, ∆SJC, ∆CXCL1, ∆β-EP, ∆TNF-α, and ∆IL-1β in the treatment group were superior to the control group (13.50 [14.50] versus 6.00 [13.00] in ∆RAI, 4.00 [3.00] versus 2.00 [4.00] in ∆SJC, 0.04 ± 0.79 ng/mL versus -0.01 ± 0.86 ng/mL in ∆CXCL1, -2.43 [5.52] pg/mg versus -0.04 [4.09] pg/mg in ∆β-EP, 3.45 [5.90] pg/mL versus 1.55 [8.29] pg/mL in ∆TNF-α, and 6.15 ± 8.65 pg/mL versus 1.28 ± 8.51 pg/mL in ∆IL-1β; all P < 0.05). Conclusion. Moxibustion can improve the joint swelling and pain symptoms in patients with RA, which may be related to the fact that moxibustion can reduce the release of inflammatory factors in patients with RA and downregulate the level of CXCL1 and increase the level of β-EP at the same time. This trial is registered with ChiCTR-IOR-17012282.

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The role of TNF-α and TNF-β gene polymorphism in the pathogenesis of Rheumatoid Arthritis

Reviews in Health Care ◽

10.7175/rhc.4254129-53 ◽

2013 ◽

Vol 4 (1) ◽

pp. 29

Author(s):

Hannan Al- Rayes ◽

Misbahul Arfin ◽

Mohammad Tariq ◽

Abdulrahman Al-Asmari

Keyword(s):

Rheumatoid Arthritis ◽

Drug Therapy ◽

Monozygotic Twins ◽

Unknown Etiology ◽

Inflammatory Disorder ◽

Promoter Polymorphisms ◽

Term Outcome ◽

Long Term Outcome ◽

Tnf Α

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder of unknown etiology that affects the synovial membrane of multiple joints. The clinical presentation of RA may vary from mild to severe with excessive erosions of periarticular bone leading to the loss of functional capacity. Both genetic and environmental factors are important in the development of this disorder. The genetic contribution to susceptibility for RA is underlined by a three-to four-fold higher concordance percentage for clinically expressed disease in monozygotic twins compared to dizygotic twins. The severity and long term outcome of RA have also been related to various genetic factors. Tumor necrosis factor (TNF), a pro-inflammatory cytokine, is involved in the pathogenesis of a variety of autoimmune disorders, including RA. A large number of studies have been undertaken to determine the role of TNF-α promoter polymorphisms in the pathogenesis of RA. On the other hand few attempts have been made to identify the association between TNF-α (lymphotoxin-alfa) polymorphism and RA. In this narrative review of published literature, an attempt has been made to determine the association between TNF-α promoter polymorphisms at positions –308, –238, –489, –857, –863 and TNF-β at +252 with respect to susceptibility to and severity of RA, as well as response to drug therapy. In spite of intra-and inter-ethnic variations, analysis of data suggests a significant role of TNF-α/TNF-β polymorphisms in determining the susceptibility/severity of RA and responsiveness to anti-TNF drug therapy. The TNF gene polymorphisms may be an interesting target for novel strategies to prevent RA and/or in its early treatment. Further studies using larger samples are needed to pinpoint the regulatory polymorphisms or haplotypes and their effects on the development of certain manifestations in RA.

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Clinical and immunological efficiency of dry carbon dioxide baths in patients with asthma and obesity at the ambulatory-polyclinic stage of rehabilitation

Bulletin physiology and pathology of respiration ◽

10.36604/1998-5029-2021-80-34-41 ◽

2021 ◽

pp. 34-41

Author(s):

A. A. Uksumenko ◽

M. V. Аntonyuk ◽

E. E. Мineeva ◽

A. V. Yurenko ◽

K. K. Khodosova

Keyword(s):

Carbon Dioxide ◽

Drug Therapy ◽

Cellular Immunity ◽

Inflammatory Cytokine ◽

Comparison Group ◽

Co2 Concentration ◽

Main Group ◽

Medical Rehabilitation ◽

Rehabilitation Treatment ◽

Tnf Α

Introduction. An important part in the rehabilitation treatment of patients with asthma associated with obesity is the ambulatory-polyclinic stage of rehabilitation that includes drug and physiotherapeutic treatment. Recently, dry carbon dioxide baths (DCDB) are increasingly used.Aim. is to assess the clinical and immunological efficiency of DCDB in the complex rehabilitation treatment of patients with asthma and obesity at the ambulatory-polyclinic stage of rehabilitation.Materials and methods. The study included 60 patients with asthma and obesity admitted to the departments of medical rehabilitation and clinical examination of scientists of the Medical Association of FEB RAS. Patients of the main group (30 subjects) received DCDB and drug therapy. Patients of the comparison group (30 subjects) received only drug therapy. The DCDB procedures were carried out using the “Reabox” device at CO2 concentration of 15-20%, a temperature of 28-30ºC, 10 procedures. The changes in symptoms, ACQ-5 test, and respiratory function were assessed. The parameters of cellular immunity CD3+, CD4+, CD8+, CD16+, CD19+ and the levels of tumor necrosis factor (TNFα), interleukins (IL) IL-2, IL-4, IL-6, IL-10, IL-17A in the blood were analyzed.Results. The achievement of asthma control took less time in patients of the main group. The improvement of bronchial patency was evidenced by the positive dynamics of spirometric indices. After DCDB therapy, an increase in suppressive activity of the cellular immunity, a decrease in the levels of pro-inflammatory cytokine IL-4, IL-17A were revealed. The TNF-α/IL-10 ratio statistically significantly changed due to the increase in the level of anti-inflammatory cytokine IL-10. In the comparison group, the positive dynamics was less pronounced.Conclusion. The use of DCDB increases the clinical and immunological efficiency of the rehabilitation of patients with asthma and obesity at the ambulatory-polyclinic stage. The clinical effect is associated with immunocorrective action, which allows achieving control of the disease in a shorter period of time.

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The role of TNF-α and TNF-β gene polymorphism in the pathogenesis of Rheumatoid Arthritis

Reviews in Health Care ◽

10.7175/rhc.v4i1.425 ◽

2013 ◽

Vol 4 (1) ◽

pp. 29-53

Author(s):

Hannan Al- Rayes ◽

Misbahul Arfin ◽

Mohammad Tariq ◽

Abdulrahman Al-Asmari

Keyword(s):

Rheumatoid Arthritis ◽

Drug Therapy ◽

Monozygotic Twins ◽

Unknown Etiology ◽

Inflammatory Disorder ◽

Promoter Polymorphisms ◽

Term Outcome ◽

Long Term Outcome ◽

Tnf Α

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder of unknown etiology that affects the synovial membrane of multiple joints. The clinical presentation of RA may vary from mild to severe with excessive erosions of periarticular bone leading to the loss of functional capacity. Both genetic and environmental factors are important in the development of this disorder. The genetic contribution to susceptibility for RA is underlined by a three-to four-fold higher concordance percentage for clinically expressed disease in monozygotic twins compared to dizygotic twins. The severity and long term outcome of RA have also been related to various genetic factors. Tumor necrosis factor (TNF), a pro-inflammatory cytokine, is involved in the pathogenesis of a variety of autoimmune disorders, including RA. A large number of studies have been undertaken to determine the role of TNF-α promoter polymorphisms in the pathogenesis of RA. On the other hand few attempts have been made to identify the association between TNF-α (lymphotoxin-alfa) polymorphism and RA. In this narrative review of published literature, an attempt has been made to determine the association between TNF-α promoter polymorphisms at positions –308, –238, –489, –857, –863 and TNF-β at +252 with respect to susceptibility to and severity of RA, as well as response to drug therapy. In spite of intra-and inter-ethnic variations, analysis of data suggests a significant role of TNF-α/TNF-β polymorphisms in determining the susceptibility/severity of RA and responsiveness to anti-TNF drug therapy. The TNF gene polymorphisms may be an interesting target for novel strategies to prevent RA and/or in its early treatment. Further studies using larger samples are needed to pinpoint the regulatory polymorphisms or haplotypes and their effects on the development of certain manifestations in RA.

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Evidence for a Blood Ganglion Barrier in the Superior Cervical Ganglion of the Rat

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100053681 ◽

1982 ◽

Vol 40 ◽

pp. 204-204

Author(s):

D. M. DePace

Keyword(s):

Blood Vessels ◽

Superior Cervical Ganglion ◽

Peripheral Nerves ◽

Time Schedule ◽

Transmission Electron ◽

Cervical Ganglion ◽

The Central Nervous System ◽

Cervical Ganglia ◽

Capillary Circulation ◽

And Control

The majority of blood vessels in the superior cervical ganglion possess a continuous endothelium with tight junctions. These same features have been associated with the blood brain barrier of the central nervous system and peripheral nerves. These vessels may perform a barrier function between the capillary circulation and the superior cervical ganglion. The permeability of the blood vessels in the superior cervical ganglion of the rat was tested by intravenous injection of horseradish peroxidase (HRP). Three experimental groups of four animals each were given intravenous HRP (Sigma Type II) in a dosage of.08 to.15 mg/gm body weight in.5 ml of.85% saline. The animals were sacrificed at five, ten or 15 minutes following administration of the tracer. Superior cervical ganglia were quickly removed and fixed by immersion in 2.5% glutaraldehyde in Sorenson's.1M phosphate buffer, pH 7.4. Three control animals received,5ml of saline without HRP. These were sacrificed on the same time schedule. Tissues from experimental and control animals were reacted for peroxidase activity and then processed for routine transmission electron microscopy.

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Intramuscular Nerve and Neuromuscular Junction Alteration In Extraocular Muscles of Diabetic Mice

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100120102 ◽

1985 ◽

Vol 43 ◽

pp. 682-683

Author(s):

Bruce R. Pachter

Keyword(s):

Diabetes Mellitus ◽

Peripheral Nerves ◽

Sudden Onset ◽

Extraocular Muscles ◽

Diabetic Patients ◽

Oculomotor Palsy ◽

Third Nerve Palsy ◽

Patients With Diabetes ◽

Intramuscular Nerve ◽

Oculomotor Nerves

Diabetes mellitus is one of the commonest causes of neuropathy. Diabetic neuropathy is a heterogeneous group of neuropathic disorders to which patients with diabetes mellitus are susceptible; more than one kind of neuropathy can frequently occur in the same individual. Abnormalities are also known to occur in nearly every anatomic subdivision of the eye in diabetic patients. Oculomotor palsy appears to be common in diabetes mellitus for their occurrence in isolation to suggest diabetes. Nerves to the external ocular muscles are most commonly affected, particularly the oculomotor or third cranial nerve. The third nerve palsy of diabetes is characteristic, being of sudden onset, accompanied by orbital and retro-orbital pain, often associated with complete involvement of the external ocular muscles innervated by the nerve. While the human and experimental animal literature is replete with studies on the peripheral nerves in diabetes mellitus, there is but a paucity of reported studies dealing with the oculomotor nerves and their associated extraocular muscles (EOMs).

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Innervation of endoneurial microvessels in human sural nerve

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100125002 ◽

1992 ◽

Vol 50 (1) ◽

pp. 920-921

Author(s):

John L. Beggs ◽

Peter C. Johnson ◽

Astrid G. Olafsen ◽

C. Jane Watkins

Keyword(s):

Blood Flow ◽

Blood Vessels ◽

Blood Supply ◽

Peripheral Nerves ◽

Sural Nerve ◽

Nerve Fibers ◽

Arterial Supply ◽

Autonomic Nerve ◽

Vasa Nervorum ◽

Endoneurial Blood Flow

The blood supply (vasa nervorum) to peripheral nerves is composed of an interconnected dual circulation. The endoneurium of nerve fascicles is maintained by the intrinsic circulation which is composed of microvessels primarily of capillary caliber. Transperineurial arterioles link the intrinsic circulation with the extrinsic arterial supply located in the epineurium. Blood flow in the vasa nervorum is neurogenically influenced (1,2). Although a recent hypothesis proposes that endoneurial blood flow is controlled by the action of autonomic nerve fibers associated with epineurial arterioles (2), our recent studies (3) show that in addition to epineurial arterioles other segments of the vasa nervorum are also innervated. In this study, we examine blood vessels of the endoneurium for possible innervation.

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Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

Clinical Science ◽

10.1042/cs20190999 ◽

2019 ◽

Vol 133 (22) ◽

pp. 2283-2299

Author(s):

Apabrita Ayan Das ◽

Devasmita Chakravarty ◽

Debmalya Bhunia ◽

Surajit Ghosh ◽

Prakash C. Mandal ◽

...

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Chronic Inflammation ◽

Ex Vivo ◽

Human Subjects ◽

Critical Role ◽

Atherosclerotic Cardiovascular Disease ◽

Tnf Α ◽

Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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