scholarly journals Pendekatan Terapi Asthma-COPD Overlap (ACO)

2019 ◽  
Vol 3 (3) ◽  
pp. 97
Author(s):  
Muhammad Amin ◽  
Alamsyah Sitepu
Keyword(s):  
Clinical Manifestations ◽  
Current Treatment ◽  
Th2 Cytokines ◽  
Jak Inhibitors ◽  
Inflammatory Phenotype ◽  
P38 Mapk Inhibitor ◽  
Th1 Cytokines ◽  
Cxcr2 Antagonists ◽  
Cd4 Lymphocytes ◽  
Mapk Inhibitor

Asthma and COPD are the most common chronic airways disease and have different clinical manifestations and treatments. Asthma is an airway inflammatory disease mediated by Th2 cytokines, CD4 + lymphocytes and eosinophils, whereas inflammation of COPD is affected by Th1 cytokines, CD8 + lymphocytes and neutrophils. Asthma-COPD overlap (ACO) is the presence of persistent airflow limitations with some symptoms resembling asthma and some other symptoms similar to COPD. Current treatment of ACO is to target the dominant inflammatory phenotype of eosinophils and neutrophils. Treatments given to patients with dominant eosinophil phenotype are inhaled and anti-IgE corticosteroids, and the drugs under reasearch are anti-IL-5, anti-IL-13, GATA3 inhibitors, anti-IL-33, anti-IL-25 and anti-thymic stromal lymphopoietin (anti-TSLP). Treatment given to patients with dominant neutrophil phenotype was macrolide, and treatment under reasearch was anti-IL-1, anti-IL-17A, anti-IL-23, CXCR2 antagonists, p38 MAPK inhibitor / JAK inhibitors and PDE4 inhibitors. Paucygranulocyte patient were given LAMA, LAMA + LABA therapy and bronchial thermoplasty. The therapy currently under study for this group is triple inhalation.

NEUROENDOCRINE TUMORS OF THE PANCREAS: ETIOLOGY, PATHOGENESIS, DIAGNOSIS, AND CURRENT TREATMENT APPROACHES

2018 ◽  
Vol 64 (6) ◽  
pp. 830-839
Author(s):  
Temuri Morgoshiya
Keyword(s):  
Neuroendocrine Tumors ◽  
Clinical Manifestations ◽  
Gastrointestinal Hormones ◽  
Current Treatment ◽  
High Potential ◽  
Long Term Results ◽  
Considerable Part ◽  
Treatment Approaches ◽  
By Products

The overview of literature on modem classification issues, diagnostics and treatments of neuroendocrinal tumors of a pancreas is provided. According to modern views all neuroendocrinal tumors of a pancreas having clinical manifestations (in the form of the syndromes caused by products of specific hormones; increases in level of hormones in blood of patients without clinical manifestations; in the form of signs of existence of volume education in various departments of PZh) and/or the researches (more than 5 mm) revealed by means of beam methods are malignant in the biology as they have high potential to innidiation. In article it is shown that a considerable part of neuroendocrinal tumors of a pancreas are nonfunctioning, i.e. not cosecreting various gastrointestinal hormones and polypeptides in blood and thereof not followed characteristic clinical manifestations. It is noted that diagnostics of neuroendocrinal tumors of a pancreas is extremely difficult task on which solution the choice of a method of treatment and its long-term results depends...

scholarly journals AB1048 RHUPUS SYNDROME IN A TERTIARY HOSPITAL

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1815.1-1815
Author(s):  
I. Martínez Cordellat ◽  
R. Gonzalez Mazario ◽  
M. De la Rubia Navarro ◽  
C. Pávez Perales ◽  
S. Leal Rodriguez ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Clinical Manifestations ◽  
Tertiary Hospital ◽  
Jak Inhibitors ◽  
Systematic Revision ◽  
Erosive Arthritis ◽  
Rheumatoid Nodules ◽  
Clinical Records ◽  
Low Prevalence ◽  
First Diagnosis

Background:Rhupus syndrome (RhS) is a rare combination of rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Different studies describe RhS cases that begin with erosive arthritis and the presence of rheumatoid factor (RF) and/or anti CCP and then the SLE symptoms.Objectives:Despite the fact that RhS shows a low prevalence, it would be useful to know clinical characteristics of RhS patients since their therapy and outcome differ from those having RA or SLE alone.Methods:Retrospective study with systematic revision of electronic clinical records of RhS patients was performed. Demographic, clinical and immunological data were collected.Results:Eight RhS patients were included (all fulfilled SLICC 2012 criteria for SLE and ACR 2010 for RA). Mean age was 67.3 (45-84) years (7 were female).In 3 cases RA was the first diagnosis with a mean evolution of 4.5 years until SLE diagnosis. In contrast, in 5 cases SLE was the first diagnosis with a mean evolution of 7.2 years until RA diagnosis. Photosensitivity and arthritis were the predominant clinical manifestations. One patient presents pericarditis and other case showed rheumatoid nodules in elbows. Renal, pulmonary or neurological affection was no reported.4 patients were under biological/JAK inhibitors therapies (2 abatacept, 1 rituximab and 1 baricitinib) with favorable response of treatment.Conclusion:In contrast to other series, only the 37.5% of our RhS cases begins with polyarticular seropositive arthritis. The 62.5% started with SLE symptoms as haematological alterations, cutaneous and serological manifestation, and showed longer progression to have polyarticular affection. Thus, RhS diagnosis is earlier in patients that begin with RA symptoms. 4 RhS patients were refractory to DMARd treatments, where biological/JAK inhibitors therapies are needed.Disclosure of Interests:None declared

Additive effects of heat and p38 mapk inhibitor treatment on melanin synthesis

2007 ◽  
Vol 30 (5) ◽  
pp. 581-586 ◽  
Author(s):  
Dong-Seok Kim ◽  
Seo-Hyoung Park ◽  
Sun-Bang Kwon ◽  
Jung-Im Na ◽  
Chang-Hun Huh ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Additive Effects ◽  
Melanin Synthesis ◽  
P38 Mapk Inhibitor ◽  
Inhibitor Treatment ◽  
Mapk Inhibitor

scholarly journals Protective effects of the p38 MAPK inhibitor SB203580 on NMDA-induced injury in primary cerebral cortical neurons

2014 ◽  
Vol 10 (4) ◽  
pp. 1942-1948 ◽  
Author(s):  
XUE-WEN LIU ◽  
EN-FEI JI ◽  
PENG HE ◽  
RUI-XIAN XING ◽  
BU-XIAN TIAN ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Cortical Neurons ◽  
Protective Effects ◽  
Cerebral Cortical Neurons ◽  
P38 Mapk Inhibitor ◽  
Mapk Inhibitor

scholarly journals Metformin combined with p38 MAPK inhibitor improves cisplatin sensitivity in cisplatin-resistant ovarian cancer

2014 ◽  
Vol 10 (5) ◽  
pp. 2346-2350 ◽  
Author(s):  
YA XIE ◽  
ZHENG PENG ◽  
MINGXING SHI ◽  
MEI JI ◽  
HONGJUN GUO ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
P38 Mapk ◽  
Cisplatin Sensitivity ◽  
P38 Mapk Inhibitor ◽  
Mapk Inhibitor

Paracoccidioidomycosis: characterization of subpopulations of macrophages and cytokines in human mucosal lesions

2018 ◽  
Vol 57 (6) ◽  
pp. 757-763 ◽  
Author(s):  
C Pagliari ◽  
L Kanashiro-Galo ◽  
A C C Jesus ◽  
M G Saldanha ◽  
M N Sotto
Keyword(s):  
Th2 Cytokines ◽  
Arginase 1 ◽  
Immunohistochemistry Analysis ◽  
Tnf Α ◽  
Ifn Γ ◽  
Mucosal Lesions ◽  
Th1 Cytokines ◽  
Necrosis Factor ◽  
Number Of Cells

AbstractMucosal lesions of paracoccidioidomycosis (PCM) are frequently described and clinically important. Macrophages are classified as M1 or M2. M1 are proinflammatory and M2 are related to chronicity. Dectin-1 recognizes β-glucan and plays an important role against fungal cells. The objective was to verify the presence of M1, M2, and dectin-1 and a possible correlation with Th1/Th2 cytokines in mucosal PCM lesions. In sum, 33 biopsies of oral PCM were submitted to histological and immunohistochemistry analysis, and positive cells were quantified. Eleven biopsies were characterized by compact granulomas (G1), 12 with loose granulomas (G2), and 10 with both kind of granulomas (G3). pSTAT-1 was equally increased in the three groups. G1 was characterized by an increased number of CD163+ macrophages. G2 presented similar number of arginase 1, iNOS, and CD163 expressing cells. G3 presented an increased number of cells expressing arginase 1 and CD163 over iNOS. G1 and G3 presented high number of cells expressing interferon (IFN)-γ; interleukin (IL) 5 was increased in G2 and G3; the expression of IL10 was similar among the three groups, and the expression of tumor necrosis factor (TNF)-α was higher in G3. G1 correlates to Th1 cytokines and pSTAT-1 and G2 correlates to Th2 cytokines. G3 presents both kinds of cytokines. We could not associate the expression of arginase-1, CD163, iNOS, and dectin-1 with the pattern of cytokines or kind of granuloma.

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