Neuropeptide Y and maternal behavior in the female native Thai chicken

Maternal care behaviors in birds include incubation and rearing behaviors. During incubating period, the hens stop laying and eating less due to food restriction as a natural fasting when compared with the rearing hens, resulting in low production of eggs and chicks. Neuropeptide Y (NPY), a neurotransmitter/neuromodulator, is very well known to be involved in food intake regulation in birds and mammals. The objective of this study is to elucidate the association between NPY and maternal behaviors in the female native Thai chicken. The distributions of NPY-immunoreactive (-ir) neurons and fibers in the brain of the incubating (INC), nest-deprived (ND), and replaced-egg-with-chicks (REC) hens at day 6 were determined utilizing immunohistochemistry technique. The results revealed that the distributions of NPY-ir neurons and fibers were observed within the septalis lateralis, nucleus rotundus, and nucleus dorsolateralis anterior thalami, with predominantly located within the the nucleus paraventricularis magnocellularis (PVN). NPY-ir fibers were located throughout the brain and the densest NPY-ir fibers were distributed in a discrete region lying close to the ventriculus tertius (third ventricle) through the hypothalamus. Changes in the number of NPY-ir neurons within the PVN of the INC, ND, and REC hens were compared at different time points (at days 6 and 14). Interestingly, the number of NPY-ir neurons within the PVN was significantly higher (P < 0.05) in the INC hens when compared with those of the ND and REC hens at day 14 but not day 6. In addition, the number of NPY-ir neurons within the PVN of the INC hens was significantly increased (P < 0.05) from day 6 to day 14 but not the ND and REC hens. These results indicated, for the first time, the asscociation between NPY and maternal behaviors in the femle native Thai chicken. Change in the number of NPY-ir neurons within the PVN during the transition from incubating to rearing behavior suggested the possible role of NPY in the regulation of the maternal behaviors in this equatorial species. In addition, the native Thai chicken might be an excellent animal model for the study of this phenomenon.     

Prevalence and clinicopathologic findings of antiphospholipid syndrome nephropathy in Thai systemic lupus erythematosus patients who underwent renal biopsies

AIM: To determine the prevalence of antiphospholipid syndrome nephropathy (APSN) in Thai systemic lupus erythematosus (SLE) patients who underwent renal biopsy and to compare the relationship of renal histopathology and other significant clinical parameters between SLE patients with and without APSN. METHODS: A retrospective analysis was undertaken in systemic lupus erythematosus patients (n = 150, 44 <15 years old, 106 0e;15 years old) who underwent renal biopsy. The specimens were evaluated for histological features of APSN and other significant clinical parameters. The result of antiphospholipid antibodies, clinical course, and renal function from chart review were analysed. RESULTS: The prevalence of APSN in systemic lupus erythematosus patients who underwent renal biopsies was 34% (16% in <15-year-old group, 41.5% in > or =15-year-old group). APSN was associated with more severe hypertension (P = 0.002 for systolic and P = 0.004 for diastolic blood pressure), acute renal failure (P = 0.003), persistent heavy proteinuria (P < 0.001 for 4+ proteinuria), severe lupus nephritis (class III and IV, P = 0.014, high activity and chronicity indices, P < 0.001) and a tendency to progress to end-stage renal disease. CONCLUSION: Systemic lupus erythematosus patients who underwent renal biopsies in our institute showed a prevalence of APSN comparable to those in western countries. The presence of APSN was significantly higher in the adult than in the paediatric population. Its association with poor prognostic indicators suggests poor renal outcome. Clinicians should be aware of this condition in order to give proper care to systemic lupus erythematosus patients.     

Thailand's national strategic plan on antimicrobial resistance: progress and challenges

Antimicrobial resistance is a serious threat that affects all countries. The Global Action Plan on antimicrobial resistance and the United Nations Political Declaration on antimicrobial resistance set standards for countries to resolve antimicrobial resistance challenges under the One Health approach. We assess progress and challenges in implementing Thailand’s national strategic plan on antimicrobial resistance 2017–2022, discuss interim outcomes and share lessons learnt. Major progress includes: establishing a national governance mechanism that leads high-impact policy on antimicrobial resistance and consolidates actions and multisectoral collaboration; creating a monitoring system and platform to track implementation of the strategic plan; and converting strategies of the strategic plan into actions such as controlling the distribution and use of antimicrobials in humans and animals. Interim results indicate that antimicrobial consumption in animals has nearly halved (exceeding the national goal of a 30% reduction) whereas other goals have not yet reached their targets. We have learnt that elevating antimicrobial resistance to high-level visibility and establishing a national governance mechanism is an important first step, and a monitoring and evaluation system should be developed in parallel with implementation. Securing funds is crucial. Policy coherence is needed to avoid duplication of actions. Highly ambitious goals, although yet to be achieved, can advance actions beyond expectations. Political commitment and collaboration across different sectors will continue to play important roles but might not be sustained without a well-designed governance structure to support long-term actions to address antimicrobial resistance.     

Immunolocalization of fibroblast growth factor-1 (FGF-1), its receptor (FGFR-1), and fibroblast-specific protein-1 (FSP-1) in inflammatory renal disease

BACKGROUND: The fibroblast growth factor (FGF) family has functions in development, cell proliferation, migration, and differentiation. While FGF-2 induces fibrosis, the role of FGF-1 in inflammation and fibrosis is less defined. We examined the expression of FGF-1 and FGF receptor (FGFR-1) to determine if renal diseases with varying etiologies of inflammation, including lupus nephritis (LN), acute interstitial nephritis (AIN) and acute rejection superimposed on chronic allograft nephropathy (CAN), showed varying patterns of expression. We also examined the expression of fibroblast-specific protein-1 (FSP-1), which has been linked to epithelial-mesenchymal transition (EMT) and fibrosis, to determine whether it was linked to potential profibrotic and inflammatory FGF-1 mechanisms. METHODS: Proliferative LN (PLN) (N= 12), nonproliferative lupus nephritis (NPLN) (N= 5), AIN (N= 6), CAN (N= 4), and normal kidneys (N= 3) were studied. FGF, FGFR-1, and FSP-1 were localized by immunohistochemistry, and intensity scored on a 0 to 3+ scale. Double staining with CD68 and separate immunohistochemical staining for CD4 and CD8 with serial sections analysis were done to identify if T lymphocytes or macrophages showed staining for FGF-1 and FGFR-1 or FSP-1. RESULTS: In normal kidneys, FGF-1 was expressed in mesangial cells (0.67 +/- 0.58), glomerular endothelial (0.67 +/- 0.58), visceral, and parietal epithelial cells (1.67 +/- 0.58). FGFR-1 showed a similar pattern of staining but also was expressed in tubular epithelium, and arterial endothelium and smooth muscle. Expression of FGF-1 was increased over normal in glomerular parenchymal cells only in CAN in podocytes (2.30 +/- 0.58 vs. 3.00 +/- 0.00) (P < 0.05) and parietal epithelial cells (1.67 +/- 0.58 vs. 2.25 +/- 0.50) (P < 0.05). Infiltrating glomerular and interstitial inflammatory cells in diseased glomeruli also expressed FGF-1 and FGFR-1. Tubular cells expressed slightly increased FGFR-1 in renal diseases vs. normal, whereas tubules remained negative for FGF-1 in diseased kidneys. FSP-1 expression was prominent in the interstitium in all kidneys with interstitial inflammation, and most prominent in CAN. Interstitial FSP-1+ cells were consistent with a myofibroblast-type morphology, and did not stain with CD-68. FSP-1 expression was closely associated with inflammatory cells expressing FGF-1 and FGFR-1. FSP-1 also showed positivity within crescents and occasional podocytes in PLN. CONCLUSION: The expression of FGF-1 and FGFR-1 in infiltrating lymphocytes and macrophages, and of FGFR-1 in tubules, is supportive, but does not prove causality, of the possibility that FGF-1 might have both autocrine and paracrine functions in renal inflammation. However, the initial stimulus for renal inflammation, whether immune complex, hypersensitivity or rejection, did not alter expression patterns of FGF-1 or its receptor. The colocalization of inflammatory infiltrates with interstitial fibrosis supports the possibility of a contribution of FGF-1 for chemotaxis and associated fibrosis, further supported by interstitial FSP-1 expression closely associated with these inflammatory cells expressing FGF-1 and FGFR-1.