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1

Muythan, Ko. Cpâp bānijjakamm. 2nd ed. [Phnom Penh]: Paṇṇagār Qaṅgar, 2007.

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2

Sākalvidyālăy Jāti Grápgraṅ. Mahāvidyālăy Nitisātr. Mūlṭhān cpâp niṅ sthāpăn cpâp = Legal principles and institutions. 2nd ed. Phnom Penh]: Mahāvidyālăy Nitisāstr, Sākalvidyālăy Jāti Grápgraṅ, 2010.

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3

Instituto Nacional de Estatística (Portugal). Estadísticas da CPLP. Lisboa: Instituto Nacional de Estatística, 2000.

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4

Ṅűy. Cpâp Kraṃ Nũy. [Phnom Penh]: Buddhasāsanapaṇḍity, 1985.

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5

plc, Barbour Index, ed. CPD briefing. Windsor: Barbour Index plc, 1995.

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6

plc, Barbour Index, ed. CPD briefing. Windsor: Barbour Index plc, 1999.

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7

plc, Barbour Index, ed. CPD briefing. Windsor: Barbour Index plc, 1996.

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8

plc, Barbour Index, ed. CPD briefing. Windsor: Barbour Index plc, 1997.

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9

Seminário "Comunidade dos Países de Língua Portuguesa-CPLP: Oportunidades e Perspectivas" (2002 Brasília, Brazil). CPLP: Oportunidades e perspectivas. Brasília, DF: IPRI, FUNAG, 2002.

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10

UNICEF--Malawi. Country programme (CPAP) 2008-2011. Lilongwe: Government of Malawi, UNICEF, 2007.

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11

Paristhānʼ, Cambodia Krasuaṅ, ed. Cpâp stībī taṃpán kārnār dhammajāti. [Phnom Penh]: Krasuaṅ Paristhān, 2008.

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12

Ūsath, Suan. Dassana vijjā cpâp =: Legal philosophy. [Phnom Penh]: Sakalvidyālăy Caṃroen Bahu Paccek Vidyā, 2007.

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13

Paristhānʼ, Cambodia Krasuaṅ, ed. Cpâp stībī taṃpán kārnār dhammajāti. [Phnom Penh]: Krasuaṅ Paristhān, 2008.

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14

Paristhānʼ, Cambodia Krasuaṅ, ed. Cpâp stībī taṃpán kārnār dhammajāti. [Phnom Penh]: Krasuaṅ Paristhān, 2008.

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15

Physiotherapy, Chartered Society of, ed. The CPD process. London: Chartered Society of Physiotherapy, 2000.

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16

Janet, Grant, Chambers Ellie, Jackson Gordon, Open University, and Joint Centre for Education in Medicine., eds. The Good CPD guide: A practical guide to managed CPD. Sutton, Surrey: Reed Healthcare Publishing, 1999.

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17

̊Kambujā, Vidyāsthān Sārakhamnākhamn. Serībhāb bartamān : kārqanket priapdhiap phnaek cpâp. Bhnạm Beñ: Vidyāsthān Sārakhamnākhamn ̊Kambujā, 2003.

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18

Majjhamaṇḍal Qápraṃ Cpâp samrâp Sahagamn ̊(Cambodia), ed. Cpâp stībī mukhrapar niṅ kārṅār Kambujā. 3rd ed. [Phnom Penh]: Majjhamaṇḍal Qápraṃ Cpâp samrâp Sahagamn̊, 2007.

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19

̊Kambujā, Vidyāsthān Sārakhamnākhamn. Serībhāb bartamān: Kārqaṅket priapdhiap phnaek cpâp. Bhnạm Beñ: Vidyāsthān Sārakhamnākhamn ̊Kambujā, 2003.

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20

Langel, Ülo. CPP, Cell-Penetrating Peptides. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8747-0.

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21

Development, United States Office of Community Planning and. CPD administrated housing rehabilitation. Washington, D.C: U.S. Dept. of Housing and Urban Development, Office of Community Planning and Development, 1989.

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22

Assurance, Institute of Quality, ed. CPD: Continuing professional development. London: Institute of Quality Assurance, 1995.

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23

Abhishek, Abhishek, and Michael Doherty. Clinical features of calcium pyrophosphate crystal deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0050.

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Calcium pyrophosphate deposition (CPPD) occurs in the elderly, and is commonly asymptomatic. However, it can cause acute calcium pyrophosphate (CPP) crystal arthritis, chronic CPP crystal inflammatory arthritis, and is frequently present in joints with osteoarthritis (OA). Acute CPP crystal arthritis presents with rapid onset of acute synovitis, which frequently affects the knees, wrists, shoulders, and elbows. It can mimic sepsis in the elderly, and may require hospital admission. Patients with CPPD plus OA may have more inflammatory signs and symptoms (e.g. joint swelling, stiffness) than those with OA alone. Additionally, patients with CPPD plus OA may also have intermittent attacks of acute CPP crystal arthritis. Some patients with CPPD may have more chronic inflammatory joint involvement and are classified as chronic CPP crystal inflammatory arthritis. This chapter describes the clinical features and differential diagnosis of common clinical manifestations of CPPD and outlines some of its rarer manifestations.
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24

Roddy, Edward, and Michael Doherty. Calcium pyrophosphate crystal deposition (CPPD). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0142.

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Calcium pyrophosphate crystal deposition (CPPD) in articular cartilage is a common age-related phenomenon. Recent important advances in our understanding of the pathophysiology of pyrophosphate metabolism include the identification of a mutation within the ANK gene which associates with familial CPPD, and elucidation of the interleukin-1β‎ (IL-1β‎)-dependent mechanisms by which crystals invoke an inflammatory response. Risk factors for CPPD include age, prior joint damage and osteoarthritis, genetic factors, and occasionally metabolic diseases (hyperparathyroidism, haemochromatosis, hypomagnesaemia, and hypophosphatasia). CPPD is commonly asymptomatic or may present as osteoarthritis with CPPD, acute calcium pyrophosphate (CPP) crystal arthritis, or chronic CPP crystal inflammatory arthritis. Although radiographic chondrocalcinosis is often taken to be synonymous with CPPD, other calcium crystals can also have this appearance and definitive diagnosis requires identification of CPP crystals by compensated polarized light microscopy of aspirated synovial fluid. Recently, the ultrasonographic appearances of CPPD have been described. Treatment of CPPD is targeted to the clinical presentation. Acute CPP crystal arthritis is treated by aspiration and injection of glucocorticosteroid, local ice packs, non-steroidal anti-inflammatory drugs (NSAIDS), low-dose colchicine, oral or parenteral glucocorticosteroids, or adrenocorticotrophic hormone (ACTH). Treatment of osteoarthritis with CPPD is very similar to the treatment of osteoarthritis alone. There is no specific therapy for chronic CPP crystal inflammatory arthritis: options include NSAID, low-dose colchicine, low-dose glucocorticosteroid, methotrexate, and hydroxychloroquine. Recommendations for the management of CPPD are derived from a small evidence base and largely based on clinical experience and extrapolation from gout. Further research into diagnosis and management including novel treatment strategies such as IL-1β‎ blockade is much needed.
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25

Abhishek, Abhishek, and Michael Doherty. Investigations of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0051.

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Joint aspiration and microscopic examination of the aspirated synovial fluid remains the gold standard for the diagnosis of calcium pyrophosphate crystal deposition (CPPD). If synovial fluid aspiration is not feasible, plain radiography and/or ultrasound scanning may be used to detect chondrocalcinosis (CC) which predominantly occurs due to calcium pyrophosphate (CPP) crystals, and this can be used as a diagnostic surrogate for CPPD as suggested by the EULAR Task Force. Acute CPP crystal arthritis often associates with a brisk acute phase response (elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), plasma viscosity) and neutrophilia. A mildly raised CRP and/or ESR may be present in chronic CPP crystal inflammatory arthritis. On the contrary, asymptomatic CC, or CPPD with osteoarthritis does not cause raised acute phase reactants. As CPPD most commonly occurs due to increasing age and osteoarthritis, investigations to screen for underlying metabolic abnormalities should be carried out in those with early-onset CPPD (under 55 years), or in those with florid polyarticular CC. As hyperparathyroidism gets more common with ageing its presence should be specifically sought in all age groups. Tests for other predisposing metabolic conditions should only be carried out in the presence of specific clinical features. Genotyping for mutations, especially in the ANKH gene, may be warranted in those with a family history of premature CPPD and no evidence of inherited metabolic predisposition, but such testing is unavailable to most clinicians.
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26

Abhishek, Abhishek, and Michael Doherty. Treatment of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0052.

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The treatment of calcium pyrophosphate crystal deposition (CPPD) is mainly symptomatic. Acute calcium pyrophosphate (CPP) crystal synovitis should be treated with rest, local application of ice packs, joint aspiration, and/or intra-articular corticosteroid injection (once joint sepsis has been excluded). Oral colchicine or prednisolone may be used if joint aspiration and/or injection are not feasible. Anti-inflammatory agents (with proton pump inhibitors) may be used but in general these should be avoided as most patients with acute CPP crystal arthritis are elderly, and at a high risk of gastrointestinal and renal complication of non-steroidal anti-inflammatory drug (NSAIDs). Principles of management of CPPD with osteoarthritis (OA) are identical to those for isolated OA. However, patients may have more inflammatory signs and symptoms and periodic joint aspiration and corticosteroid injection may be required more often than in isolated OA. Oral NSAIDs (with gastro-protection), colchicine, low-dose corticosteroids, hydroxychloroquine, and radiosynovectomy have been suggested as options for the treatment of chronic CPP crystal arthritis. There is growing interest in use of anti-interleukin-1 agents for acute or chronic CPP crystal arthritis but the efficacy of these agents has not been formally studied, and their use should be considered on an individual basis.
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27

CPEP Biology (College Proficiency Examination Program) (Cpep-5). National Learning Corp, 2000.

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28

Goodbye Cpap: CPAP Alternative Sleep Apnea Treatment Options. Independently Published, 2020.

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29

Mulligan, Tim. Goodbye CPAP Goodbye Sleep Apnea: Healthy Sleep Without CPAP. Independently Published, 2021.

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30

Cpâp stībī braijhoe. [Phnom Penh: s.n.], 2010.

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31

Mitchell, Jennifer K. Navigating the Cplp. ASTD Press, 2006.

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32

Cpâp stībī jalphal. [Phnom Penh: s.n.], 2006.

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33

Rudman, Jack. Economics (Cpep-8). National Learning Corp, 1997.

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34

MD, Yatin J. Patel. CPAP is Sexy: Get Lasting Vigor & Vitality from Your CPAP. CreateSpace Independent Publishing Platform, 2017.

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35

CPD briefing. Windsor: Barbour Index plc, 1998.

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36

Publication, Newbee. CPD Journal. Independently Published, 2020.

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37

UK Chamber of Shipping Staff, Witherby Publishing Group, and ECDIS Ltd Staff. ECDIS CPD. Witherby & Company, 2019.

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38

Cpâp stībī kārtruatbinity grẏanñian. [Phnom Penh: s.n.], 2007.

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39

Cpâp stībī kārtruatbinity grẏanñian. [Phnom Penh: s.n.], 2007.

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40

Beat Cop: Cpop 1986. Van Velzer Press, 2022.

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41

Rudman, Jack. Freshman English (Cpep-11). National Learning Corp, 1997.

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42

Rudman, Jack. Regents College Proficiency Examination Series (Cpep (Regents College Proficiency Examination Series (Cpep).). Natl Learning Corp, 1997.

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43

Rudman, Jack. Regents College Proficiency Examination Series (Cpep (Regents College Proficiency Examination Series (Cpep).). Natl Learning Corp, 1997.

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44

HONEYCUTT, Rachel. Final Planning Book: Snoring CPAP As a Fighter Pilot Mask Funny CPAP. Independently Published, 2021.

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45

HONEYCUTT, Rachel. Reading List Book: Snoring CPAP As a Fighter Pilot Mask Funny CPAP. Independently Published, 2021.

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46

Hill, J. D., Glynn Rhodes, and Steve Volalr. Car Park Designers' Handbook, 2nd Ed. Thomas Telford Ltd, 2013. http://dx.doi.org/10.1680/cpdh.58149.

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47

HONEYCUTT, Rachel. Self Care Acts Planner: Snoring CPAP As a Fighter Pilot Mask Funny CPAP. Independently Published, 2021.

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48

HONEYCUTT, Rachel. Family Refrigerator Inventory List: Snoring CPAP As a Fighter Pilot Mask Funny CPAP. Independently Published, 2021.

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49

Walder, Dave, and Paul Reading. Narcolepsy: still sleepy on CPAP. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0011.

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Sleep disorders are an increasingly common reason for referral to the respiratory clinic, and our understanding of the different aetiologies is increasing. The commonest sleep disorder is sleep apnoea, but other sleep disorders can cause similar symptoms. Narcolepsy is a neurological disorder that affects the brain’s ability to regulate the normal sleep-wake cycle and often presents with similar symptoms to obstructive sleep apnoea, daytime hypersomnolence, and disturbed night-time sleeping but is largely underdiagnosed. This chapter discusses a patient who presented with symptoms of daytime somnolence and witnessed apnoeas and details the investigations required for a diagnosis of narcolepsy. It covers the more specialized sleep studies required for a clinical diagnosis and the treatment options available for patients with this condition.
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50

Cpâp stībī taṃpán kārnār dhammajāti. [Phnom Penh]: Krasuaṅ Paristhān, 2008.

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