Treatment of the chronic inflammation in peripheral target tissue improves the crushed nerve recovery in the rat

2002 ◽  
Vol 202 (1-2) ◽  
pp. 69-74 ◽  
Author(s):  
Naoki Kato ◽  
Koichi Nemoto ◽  
Hiroshi Arino ◽  
Kyosuke Fujikawa
Keyword(s):  
Chronic Inflammation ◽  
Peripheral Target ◽  
Target Tissue ◽  
Nerve Recovery ◽  
Crushed Nerve

Influence of chronic inflammation in peripheral target tissue on recovery of crushed nerve injury

2001 ◽  
Vol 6 (5) ◽  
pp. 419-423 ◽  
Author(s):  
Naoki Kato ◽  
Koichi Nemoto ◽  
Masahisa Kawaguchi ◽  
Masatoshi Amako ◽  
Hiroshi Arino ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Nerve Injury ◽  
Peripheral Target ◽  
Target Tissue ◽  
Crushed Nerve

FAILURE OF DIHYDROTESTOSTERONE TO ELICIT SEXUAL BEHAVIOUR IN THE FEMALE CAT

1977 ◽  
Vol 75 (1) ◽  
pp. 173-174 ◽  
Author(s):  
VERONICA A. CERNY
Keyword(s):  
Sexual Behaviour ◽  
Female Rats ◽  
University Of Pennsylvania ◽  
Male Rat ◽  
Peripheral Target ◽  
Target Tissue ◽  
Male And Female ◽  
Behavioural Effects ◽  
Male And Female Rats ◽  
Target Organs

Laboratory of Anatomy, Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, U.S.A. (Received 28 March 1977) Testosterones have stimulatory effects on peripheral target tissue and sexual behaviour in male and female rats (Beach, 1942), guinea-pigs (Young, 1961; Diamond & Young, 1963), rabbits (Palka & Sawyer, 1966; Beyer & Rivaud, 1973) and cats (Green, Clemente & de Groot, 1957; Young, 1961; Whalen & Hardy, 1970). 5α-Androstan-17β-ol-3-one (dihydrotestosterone, DHT) has stimulatory effects on peripheral target organs, and like testosterones, a negative feedback effect on the pituitary gland and hypothalamus (Feder, 1971). No behavioural effects were seen in male or female rats when DHT was injected systemically (Beyer, Morali & Cruz, 1971; Feder, 1971) nor in the male rat when it was administered intracerebrally (Johnston & Davidson, 1972). Many experiments support the hypothesis that only androgens that can be aromatized to oestrogens can elicit sexual behaviour and

scholarly journals SP prevents T2DM complications by immunomodulation

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Sang-Min Baek ◽  
Kiyoung Kim ◽  
Suna Kim ◽  
Youngsook Son ◽  
Hyun Sook Hong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Bone Marrow ◽  
Stem Cell ◽  
Chronic Inflammation ◽  
Systemic Inflammation ◽  
Bone Marrow Stem Cell ◽  
The Body ◽  
Target Tissue ◽  
Oletf Rats ◽  
Marrow Stem Cell

Abstract Type 2 diabetic mellitus (T2DM) is characterized by systemic inflammation and insulin resistance due to obesity, and this leads to critical complications, including retinopathy and nephropathy. This study explored the therapeutic effect of substance-p (SP), a neuropeptide, on T2DM progression and its complications. To examine whether SP affects glucose metabolism, lipid metabolism, systemic inflammation, and retinopathy, Otsuka Long-Evans Tokushima Fatty rats (OLETF, 27 weeks old) with chronic inflammation, obesity, and impaired bone marrow stem cell pool was selected. SP was intravenously injected and its effect was evaluated at 2 and 4 weeks after the SP injection. OLETF had typical symptoms of T2DM, including obesity, chronic inflammation, and poor glycemic control. However, SP treatment inhibited the body-weight gain and reduced circulating levels of free fatty acid, cholesterol, and triglyceride, ameliorating the obese environment. SP could suppress inflammation and rejuvenate bone marrow stem cell in OLETF rats. SP-mediated metabolic/immunological change could resolve hyperglycemia and insulin resistance. Histopathological analysis confirmed that SP treatment alleviated the dysfunction of target tissue with insulin resistance. OLETF rats have retinal damage from 27 weeks of age, which was reliably aggravated at 31 weeks. However, SP treatment could restore the damaged retina, sustaining its structure similarly to that of non-diabetic rats. In conclusion, systemic application of SP is capable contribute to the inhibition of the progression of T2DM and diabetic retinopathy.

Acetaminophen: Macula densa hypersecretory activity by induced hepatotoxicity

1987 ◽  
Vol 45 ◽  
pp. 934-935
Author(s):  
S.S. Poolsawat ◽  
C.A. Huerta ◽  
S.TY. Lae ◽  
G.A. Miranda
Keyword(s):  
Cell Proliferation ◽  
Liver Function ◽  
Chronic Inflammation ◽  
Foam Cell ◽  
Term Effect ◽  
Short Term ◽  
Drug Induced ◽  
Experimental Induction ◽  
Tissue Alterations ◽  
Toxic Responses

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.

Nuclear receptors in disease: the oestrogen receptors

2004 ◽  
Vol 40 ◽  
pp. 157-167 ◽  
Author(s):  
Maria Nilsson ◽  
Karin Dahlman-Wright ◽  
Jan-Åke Gustafsson
Keyword(s):  
Nuclear Receptors ◽  
Target Genes ◽  
Receptor Subtype ◽  
Target Tissue ◽  
Oestrogen Receptors ◽  
Nucleotide Polymorphisms ◽  
Cell Type ◽  
Single Nucleotide ◽  
Beneficial Effects ◽  
The Family

For several decades, it has been known that oestrogens are essential for human health. The discovery that there are two oestrogen receptors (ERs), ERalpha and ERbeta, has facilitated our understanding of how the hormone exerts its physiological effects. The ERs belong to the family of ligand-activated nuclear receptors, which act by modulating the expression of target genes. Studies of ER-knockout (ERKO) mice have been instrumental in defining the relevance of a given receptor subtype in a certain tissue. Phenotypes displayed by ERKO mice suggest diseases in which dysfunctional ERs might be involved in aetiology and pathology. Association between single-nucleotide polymorphisms (SNPs) in ER genes and disease have been demonstrated in several cases. Selective ER modulators (SERMs), which are selective with regard to their effects in a certain cell type, already exist. Since oestrogen has effects in many tissues, the goal with a SERM is to provide beneficial effects in one target tissue while avoiding side effects in others. Refined SERMs will, in the future, provide improved therapeutic strategies for existing and novel indications.

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

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.

Nanotheranostic agents for neurodegenerative diseases

2020 ◽  
Vol 4 (6) ◽  
pp. 645-675
Author(s):  
Parasuraman Padmanabhan ◽  
Mathangi Palanivel ◽  
Ajay Kumar ◽  
Domokos Máthé ◽  
George K. Radda ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Neurodegenerative Diseases ◽  
Cell Types ◽  
Specific Cell ◽  
Ageing Population ◽  
Target Tissue ◽  
Therapeutic Approaches ◽  
Surface Receptors ◽  
Theranostic Agents ◽  
Preclinical Animal Models

Neurodegenerative diseases (NDDs), including Alzheimer's disease (AD) and Parkinson's disease (PD), affect the ageing population worldwide and while severely impairing the quality of life of millions, they also cause a massive economic burden to countries with progressively ageing populations. Parallel with the search for biomarkers for early detection and prediction, the pursuit for therapeutic approaches has become growingly intensive in recent years. Various prospective therapeutic approaches have been explored with an emphasis on early prevention and protection, including, but not limited to, gene therapy, stem cell therapy, immunotherapy and radiotherapy. Many pharmacological interventions have proved to be promising novel avenues, but successful applications are often hampered by the poor delivery of the therapeutics across the blood-brain-barrier (BBB). To overcome this challenge, nanoparticle (NP)-mediated drug delivery has been considered as a promising option, as NP-based drug delivery systems can be functionalized to target specific cell surface receptors and to achieve controlled and long-term release of therapeutics to the target tissue. The usefulness of NPs for loading and delivering of drugs has been extensively studied in the context of NDDs, and their biological efficacy has been demonstrated in numerous preclinical animal models. Efforts have also been made towards the development of NPs which can be used for targeting the BBB and various cell types in the brain. The main focus of this review is to briefly discuss the advantages of functionalized NPs as promising theranostic agents for the diagnosis and therapy of NDDs. We also summarize the results of diverse studies that specifically investigated the usage of different NPs for the treatment of NDDs, with a specific emphasis on AD and PD, and the associated pathophysiological changes. Finally, we offer perspectives on the existing challenges of using NPs as theranostic agents and possible futuristic approaches to improve them.

Clinical Update: Assessing Maximum Medical Improvement in Carpal Tunnel Syndrome

2003 ◽  
Vol 8 (4) ◽  
pp. 4-5
Author(s):  
Christopher R. Brigham ◽  
James B. Talmage
Keyword(s):  
Carpal Tunnel Syndrome ◽  
Carpal Tunnel ◽  
Proper Time ◽  
Carpal Tunnel Release ◽  
Hand Function ◽  
Factors Affecting ◽  
Early Results ◽  
Medical Evaluation ◽  
Nerve Recovery ◽  
Tunnel Syndrome

Abstract Permanent impairment cannot be assessed until the patient is at maximum medical improvement (MMI), but the proper time to test following carpal tunnel release often is not clear. The AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) states: “Factors affecting nerve recovery in compression lesions include nerve fiber pathology, level of injury, duration of injury, and status of end organs,” but age is not prognostic. The AMA Guides clarifies: “High axonotmesis lesions may take 1 to 2 years for maximum recovery, whereas even lesions at the wrist may take 6 to 9 months for maximal recovery of nerve function.” The authors review 3 studies that followed patients’ long-term recovery of hand function after open carpal tunnel release surgery and found that estimates of MMI ranged from 25 weeks to 24 months (for “significant improvement”) to 18 to 24 months. The authors suggest that if the early results of surgery suggest a patient's improvement in the activities of daily living (ADL) and an examination shows few or no symptoms, the result can be assessed early. If major symptoms and ADL problems persist, the examiner should wait at least 6 to 12 months, until symptoms appear to stop improving. A patient with carpal tunnel syndrome who declines a release can be rated for impairment, and, as appropriate, the physician may wish to make a written note of this in the medical evaluation report.

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