Showing posts with label Biochemistry. Show all posts
Showing posts with label Biochemistry. Show all posts

03 October 2014

Hyperphosphatemia Ppts and latest published articles



Hyperphosphatemia: Hyperphosphatemia is an electrolyte disturbance in which there is an abnormally elevated level of phosphate in the blood.

Chronic Kidney Disease
Sandeep Vetteth
https://www.utoledo.edu

Vascular Calcification
Kristina Boström, MD, PhD
https://www.mcdb.ucla.edu/VBTG/VascCalc_Bostrom.ppt

Hem/Onc Emergencies
Peter Newburger, MD, Venee Tubman, MD
https://www.umassmed.edu

The Cellular Environment: Fluids and Electrolytes, Acids and Bases
http://users.ipfw.edu

Dyatrophic Calcinosis
Dr Abdelaziz Elamin, MD, PhD
http://www.pitt.edu/

Functions of the Kidneys 
http://www.austincc.edu

Chronic Renal Failure
http://www.hsc.unt.edu

Regulation of Phosphate Transport in Proximal Tubule
Alexander Usorov, MD
http://medicine.med.nyu.edu

Nephrology Grand Rounds
http://medicine.med.nyu.edu

Minerals
Dr Reed Berger
https://www.uic.edu/depts/mcam/nutrition/ppt/Minerals1_add.ppt

Hem/Onc Emergencies
Saulius Girnius
http://www.bumc.bu.edu

Fluid, Electrolyte & Acid-Base Balance
http://academic.evergreen.edu

Polycystic Kidney Disease
http://www.smccd.net

Stressors Affecting
Fluid & Electrolyte Balance
K. Burger, MSEd, MSN, RN, CNE
http://www2.sunysuffolk.edu

Chronic Renal Failure
Matt Crowley, Doug Srygley , Vijay Reddy
https://vmw-lmsc.duhs.duke.edu

Electrolyte Abnormalities in the Hospitalized Patient
Cynthia Seitz MD
http://medicine.nevada.edu

Kidney Function & Disease
McCafferty
http://www.csuchico.edu

200 Latest Published articles of Hyperphosphatemia

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03 December 2013

Lipid spectrum



Lipid spectrum 

Mass Spectrometry meets Cheminformatics
Tobias Kind and Julie Leary
http://fiehnlab.ucdavis.edu

Development of a NMR-based Metabolomics Analysis Methodology for Toxicology
Jahns, G.L., Reo, N.V., Kent, M.N., Burgoon, L.D., Zacharewski, T.R., DelRaso, N
http://www.bch.msu.edu

IR Spectrum of Healthy Human Hair with Expected Lipid Peak 
http://scv.bu.edu

HDL Cholesterol No Longer Is Good Cholesterol: Emerging Genetic Theories 
Sunita Dodani & Janice S Dorman
http://www.pitt.edu

Lipids and Membranes
https://soweb.as.arizona.edu

Tutorial on Computational Optical Imaging
David J. Brady
http://www.disp.duke.edu

Biomedical Raman Spectroscopy
Jason T. Motz
http://engineering.tufts.edu

Coronary Artery Disease
Punit Goel, MD
http://medicine.missouri.edu

Who Needs Photons When You Have Mass? - ACCA Spectroscopy Series
Bruce Solka, Ph.D.
http://www.stfrancis.edu/ 

Latest 225 Published articles on Lipid spectrum

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26 August 2012

Cerebrospinal fluids



Central Nervous System
http://zircon.mcli.dist.maricopa.edu

Cerebral Spinal Fluid & The Meninges
http://faculty.sdmiramar.edu

Cerebrospinal Fluid Dennis Stevens
http://chua2.fiu.edu/

Urinalysis and Body Fluids
http://www.austincc.edu/

CSF Physiology and Cerebral Blood Flow
Keith R. Lodhia, MD,MS
https://wiki.umms.med.umich.edu/

Cerebrospinal fluid (CSF)
http://www.uta.edu/

CSF Functions
http://36-454-f11.wiki.uml.edu/

CSF tau
Chris Clark
http://www.alz.washington.edu/

Brain Tidbit I:  Nourishment to the brain
http://larryfrolich.com/anatomyphysiologyone

Body Fluids
http://www9.georgetown.edu

Lumbar Puncture
http://www.meddean.luc.edu

Review CSF analysis in meningitis
http://www.med.unc.edu

Hydrocephalus
By: Abraham, De La Garza and Liana Sencion
http://www.laredo.edu


151 Published articles of CSF

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26 May 2012

Body fluid analysis



Body Fluids
BodyFluid.ppt

Pleural, Peritoneal, Pericardial Fluids
BFSerous.ppt

Synovial Fluid
BFSynovial.ppt

Blood Borne Pathogens
Blood Borne Pathogens.ppt

Introduction to Forensic Science and Criminalistics
Peter Bilous
Biological Evidence Serology.ppt

Medical Laboratory Science - The Hidden Profession
Kimberly A. Whiter MLS
MLSProfessionPresentation.ppt

Role of Body Fluid Volume Regulation
Robert W. Schrier, MD
Role of Body Fluid Volume Regulation.ppt

ASSESSMENT OF NUTRITIONAL STATUS
Abdelaziz Elamin, MD, PhD, FRCPCH
ASSESSMENT OF NUTRITIONAL STATUS.ppt

Bloodborne Pathogen Training
BloodbornePathogenTraining.ppt

Forensic DNA Analysis
Forensic DNA Analysis.ppt

The Impaired Physician Focus on Substance Abuse
Michael J. Reichgott, MD, PhD
Focus on Substance Abuse.ppt

The Effects of the Menstrual and Lunar Cycles on Body Fluid Balance
Amy J. Reckard LAT, ATC
Menstrual and Lunar Cycles on Body Fluid Balance.ppt

Blood and body fluid exposures
ohcExposureBBF.ppt

Bloodborne Pathogens
Bloodborne Pathogens.ppt

Identification of Biological Fluids and Stains
EBiolFluids.ppt

Bloodborne Pathogens (BBPs)
BBPS.ppt

FLUID AND ELECTROLYTES
FLUID AND ELECTROLYTES.ppt

Forensic Serology Identification Using Blood Groups
Forensic Serology Identification.ppt

FLUID, ELECTROLYTE, AND ACID-BASE BALANCE
FLUID, ELECTROLYTE, AND ACID-BASE BALANCE.PPT

Human DNA Quantification using qPCR
Human DNA Quantification using qPCR.ppt

Introduction to Clinical Laboratory Practices
UASedCrystals.ppt

AIDS/HIV UPDATE
Neal R. Chamberlain, Ph.D
AIDSupdate.ppt
Latest 10 published articles

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28 March 2012

Hypernatremia



Hypernatremia or hypernatraemia is an electrolyte disturbance that is defined by an elevated sodium level in the blood.

Hyponatremia and Hypernatremia
Conor Gough
Hyponatremia_and_Hypernatremia.ppt

Hypernatremia
K. Mae Hla, M.D., M.H.S.
Hypernatremia.ppt

Electrolyte Abnormalities
Cynthia Seitz MD
ElectrolyteAbnormalitiesintheHospitalizedPatient.ppt

Fluid, Electrolyte and Acid-Base Balance
Linda A. Martin, MSN APRN, BC, CNE
FluidElectrolytesAcidBase.ppt

Electrolyte Emergencies Hyponatremia Decreased serum sodium
Electrolyte Emergencies Hyponatremia.ppt

Fluid and Electrolyte Imbalances
fluid-electrolyte-3.ppt

Electrolytes
ELECTROLYTES.ppt

Drugs for Fluid Balance, Electrolyte and Acid-Base Balance
Drugs for Fluid Balance Acid-Base.ppt

Fluid & Electrolyte Imbalance
Fluid & Electrolyte Imbalance.ppt

Fluid & Electrolytes
Stuart L. Goldstein MD
Fluid & Electrolytes.ppt

Brain Response to Hypernatremia
TJ O’Neill
Brain Response to Hypernatremia.ppt

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09 March 2012

Prothrombin



Prothrombin mutations:  thrombophilic mechanisms and an unusual variant
Noah Hoffman
Prothrombin.ppt

Lupus  Anticoagulant Jennifer  Kirkland
Special_hematology/lupus_anticoagulant.ppt

Aspartate transcarbamoylase
Aspartate transcarbamoylase Lec12.ppt

Anticoagulants
Danielle Welschmeyer
Anticoagulants_DanielleWelschmeyer.ppt

Oral  Anticoagulant Therapy
Benedict  R. Lucchesi, M.D., Ph.D.
Oral  Anticoagulant Therapy.ppt

Coagulation Modifier Drugs
CoagulationModifierDrugs.ppt
Newer  Anticoagulant Therapies
Chris Ferrell MT(ASCP), CLS/H(NCA)
AdvAnticoagTherapy.ppt

Thrombin generation assays: a brief review of the literature
Noah Hoffman
NH_thrombin_2006.ppt

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29 February 2012

Lactate dehydrogenase - LDH Ppts




LDH is most often measured to check for tissue damage. The enzyme LDH is in many body tissues, especially the heart, liver, kidney, skeletal muscle, brain, blood cells, and lungs.

Lactate Dehydrogenase
By: Nancy Duong,  Julia Crawford, & Kim Luu
http://crab.rutgers.edu/~peterpal/Presentation1.ppt

Pyruvate  - Lactate  Which one  ends Glycolysis?
http://www.tamu.edu/faculty/eharris/411_602/Tutorials/Pyruvate%20-%20Lactate.ppt

Protein function
http://faculty.swosu.edu/tim.hubin/Biochem/chapt06b_lecture.ppt

Protein  Purification
http://biochem.ncsu.edu/faculty/brown/Protein%20Purification%20%202008.ppt

Glycogen Metabolism
http://www.chem.wwu.edu/prody/glycmet.ppt

General  Pathways of Metabolism
http://www.med.ufl.edu/biochem/rcohen/glycolysis.ppt

Biochemistry of Metabolism
http://www.rpi.edu/dept/bcbp/molbiochem/MBWeb/mb1/part2/8-glycolysis.ppt

Determinants of Gene Duplicability
http://www.pitt.edu/~super7/24011-25001/24991.ppt

Carbohydrate and Sugar structure
http://www.uh.edu/sibs/faculty/glegge/lecture_22a.ppt

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03 January 2011

Electrolyte Abnormalities



Electrolyte Abnormalities

Electrolyte Abnormalities in the Hospitalised Patient

Electrolytes and Acid base Disorders

Fluids & Electrolites

Fluids & Electrolytes

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31 October 2010

Blood Brain Barrier: Structure, Function and Bypass by Microorganisms



Discovery
What is the Blood Brain Barrier?
Structure of Blood Brain Barrier
Integrity of BBB
Astrocyte end feet
Tight Junctions between BMEC
Claudin
Occludin
Barrier Function of Occludin and Claudin
Junction Adhesion Molecules:
BMEC intercellular space
Barrier function of JAM
Cytoplasmic accessory proteins
Membrane associated guanylate kinase-like proteins (MAGUKS)
Adherens Junction
Pericytes
Astrocyte end feet
Circumventricular organs
Circumventricular organ functions:
Normal BBB transport
Factors produced by astrocytes
Glutamate,
Aspartate
Taurine
ATP
Endothelin-1
NO
MIP-2
Tumor necrosis factor alpha TNF-α
Interleukin beta IL-β
Bradykin
5HT
Histamine
Thrombin
UTP
UMP
Substance P
Qionolonic acid
Platelet activating factor
Free radicals
E. Coli model
Physical damage of BBB
Ligand receptor interactions followed by host cell actin cytoskeletal rearrangements
Transcellular transport while maintaining integrity of BMEC
Physcial damage of BBB
Conclusion
References



Blood Brain Barrier: Structure, Function and Bypass by Microorganisms Download

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21 April 2010

Complex Carbohydrates



Complex Carbohydrates

- Know the structural components and differences between the glycoconjugate types
- Know the general biosynthetic and catabolic strategies and molecules involved
- Know the general function of each class of glycoconjugate
- Know the general biochemical principles associated with diseases resulting from defects in the catabolic pathways of the glycoconjugates

* Marks, Marks and Smith Chapter 30, primary source, Harper’s Ch 56 supersecondary source. Review Ch. 15,16 for sugar and lipid structural properties

General Biosynthetic and Catabolic Themes for Glycoconjugates
* An initial sugar residue is attached to a core protein or lipid, usually through a serine or asparagine residue.
* Sugar residues are added sequentially from nucleotide diphosphate sugar donors by specific glycosyltransferases in the endoplasmic reticulum and golgi.
* Glycosidases (sugar specific hydrolases) in the lysosome are responsible for degradation and catabolism
* Almost all diseases related to glycoconjugates result from defective lysosomal glycosidase function

UDP-Glucose Glycosyltranserase Reaction
Sugar Nucleotide Conversions
Proteoglycans
* Consist of a core protein, that is either transmembranous or secreted. Via serine residues, long, unbranched, repeating disaccharides of uronic acid (glucuronic or iduronic) and hexosamine (N-acetylglucosamine or N-acetylgalactosamine) are covalently attached to the protein on the (on the extracellular surface if membrane attached).
* These residues are frequently sulfated following polymer formation. Thus they possess a large net negative charge, are highly hydrated, and occupy a large amount of space extracellularly (good for their role as lubricants and molecular sieves). They also provide a large surface area for binding of other matrix components and some growth factors.
* Major components of the extracellular matrix, also in joint synovial fluid, vitreous humor of the eye, arterial walls, bone and cartilage

The main classes of disaccharide repeats found in glycosaminoglycans attached to protein
GAG-Carbohydrate Core Linkage to Protein

Sequential Biosynthetic Pathway for GAGs
Glycoproteins
There are three major classes of glycoproteins – those with carbohydrate chains that are N-linked (via an Asn), O-linked (via Ser or Thr) or linked via a glycosylphosphatidylinositol (GPI) lipid. These are primarily transmembranous proteins with the carbohydrates positioned extracellularly, and they are also secreted.

* For N-linked, the carbohydrate core structure is synthesized processively on an activated lipid carrier, dolichol phosphate, and transferred co-translationally to membrane proteins synthesized in the endoplasmic reticulum.

Three Main Types of Glycoprotein Structures
O-linked
N-linked
GPI-linked
GPI = glycosylphosphatidylinositol
Also: targeting signal for removal of damaged or mis-folded proteins from the cell
And: generally function to aid in the proper conformation and stability of membrane-associated proteins
Dolichol-linked Donor Oligosaccharide Synthesis for N-linked Glycoproteins
O-linked Glycoproteins (Mucins most common)
Glycolipids
* Carbohydrates are attached to ceramide (a sphingolipid: sphingosine plus fatty acid). Involved in cell-cell contact/interactions. The terminal carbohydrates can frequently be identical to carbohydrate chains on glycoproteins (Ex: blood group antigens)
* Cerebrosides – glycolipids with one or two sugars (glucose and galactose); if sulfated, are termed sulfatides, found in high concentrations in the brain
* Gangliosides – glycolipids that contain sialic acid residues, longer and branched relative to cerebrosides

Glycolipid Structural
Components
Sulfate donor
R = protein or ceramide
Bacteria sp. with binding proteins (lectins) for Lactosylceramide
I-Cell Disease Summary
Tay-Sachs Disease (Ex.)
* The most common form of GM2 gangliosidosis; the GM2 ganglioside accumulates due to a defect in hexosaminidase A. Causes swelling and loss of ganglion cells in the cerebral cortex, proliferation of glial cells, and demyelination of peripheral nerves.
* Rare defect in general population, but occurs 1 in every 3600 births in the U.S. Jewish population descended from Eastern Europe (ex: 1 in 28 Ashkenazi Jews carry the defect).
* No effective treatments; genetic counseling and screening are the primary approaches used to minimize occurrence.

Complex Carbohydrates

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24 March 2010

Assessment of Protein Status



Assessment of Protein Status
FCSN 442 - Nutrition Assessment Laboratory
By:Dr. David L. Gee
Central Washington University

Assessment of Protein Status
* Anthropometric Assessment
o body composition estimations
o midarm muscle circumference/area
* Laboratory Assessment
o serum albumin
o other serum proteins (transferrin, prealbumin, retinol-binding protein)
o urinary creatinine excretion
o total lymphocyte count

Midarm Muscle Area
* Estimate of MAMA is an estimate of overall muscle mass
* Assumptions

Midarm Muscle Circumference
* MAMC = AC - (.314 x TSF)

* “…change in arm muscle area is greater than the change in mid-arm circumference. Consequently, changes in upper-arm musculature are not as easily detected by measurement of mid-arm circumference as by AMA. Therefore, AMA is the preferred nutritional index.”

Arm Muscle Area
* AMA = ((MAC - (3.14 x TSF)2 ) / (4 x 3.14)
* adjusted AMA

Guidelines for Interpreting Percentile Values for Arm Muscle Area (appendix R)
Biochemical Assessment of Protein Status
* Two protein compartment model
* “No single test or group of tests can be recommended at this time as a routine and reliable indicator of protein status.” Young, 1990
* “…a combination of measures can produce a more complete picture of protein status.”

Serum Albumin
* Major serum protein
* Most common indicator of depleted protein status
* Half life = 14-20 days
* poor indicator of early protein depletion and repletion
* Levels affected by rate of synthesis (liver disease may reduce levels)
* May reflect level of physiological stress
* Levels affected by abnormal losses
* Levels affected by fluid status
* Normal values: 4.5 g/dL + 35-50 (SD)

Serum Transferrin
* Function: transport protein for iron
* half-life = 8-9 days
* Influenced by other factors
* limited usefulness in protein status assess.

Serum Prealbumin
* aka. transthyretin and thyroxine-binding prealbumin
* functions:
* short half life (2-3d), small body pool
* Returns to normal at beginning of nutritional therapy
* Influenced by other factors
* generally considered preferable than albumin and transferrin

Retinol Binding Protein
* Function: carrier for retinol
* responds like prealbumin
* very rapid turnover (12 hours), very small body pool
* generally not considered to be more useful than prealbumin

Immunocompetence
* Immune system affected by nutritional status
* Tests of immunocompetence useful functional indicators of nutritional status
* Delayed Cutaneous Hypersensitivty (DCH)
o intradermal injection of antigens
* Total Lymphocyte Count (TLC)

Total Lympocyte Count
* White blood cell count
* TLC = (%lymp x WBC)x100
* Normal = 1200-1800 cells/mm3
* Moderate PCM = 800-1200
* Severe PCM = < 800 Urinary Creatinine Excretion * Creatinine excreted in proportion to muscle mass * LBM estimated by comparing 24-hr urine creatinine excretion with standard based on stature or reference values of 23 and 18 mg/kg for M and F Example: Creatinine Height Index * CHI = (24 hr urine creatinine x 100) / (expected 24 hr urine creatinine for height) o CHI = 1436/1596 x 100 = 90% * expected values in table 9-1 (p306) o CHI > 80% = normal
o CHI = 60-80% = mild protein depletion
o CHI = 40-60% = moderate depletion
o CHI < 40% = severe depletion Assessment of Protein Status

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10 May 2009

Overview of carbohydrate metabolism



Overview of carbohydrate metabolism
Presentation by: Dr. Nuran Ercal

GLYCOLYSIS
* Glycolysis occurs in almost every living cell.
* It occurs in cytosol.
* It was the first metabolic sequence to be studied.
* Most of the work done in 1930s by the German biochemist G. Embden Meyerhof Warburg.
* That is why it is also called Embden-Meyerhof pathway.
* It is a greek word.
* Glykos------> sweet
* Lysis-------> loosing
* Glycolysis-----------> loosing or splitting of glucose
* Glc is an important fuel for most organisms.
* Why is Glc chosen?
* 1) Glc is one of the monosaccarides formed formaldehyde
* under prebiotic conditions.
* 2) Glc has a low tendency to glycosylate proteins
* Fermentations provide usable energy in the absence of oxygen
* Why is a relatively inefficient metabolic pathway so extensively
* used?
* Answer: It does not require oxygen
* Obligate anaerobes
* Facultative anaerobes
* 3 of the reactions of glycolysis are irreversible.
* Pyruvate is the end product of glycolysis in tissues with mitochondria.
* This series of 10 reactions called aerobic glycolysis,

Stages of glycolysis
* Stage I
* Goal: To trap the Glc in the cell

IMPORTANCE OF PHOSPHARYLATED INTERMEDIATES
PHOSPHORYLATION OF GLUCOSE
Induced fit in Hexokinase
Difference between hexokinase and glucokinase
Hexokinase vs glucokinase
SUMMARY
More about HK
* Hexokinase, like adenylate kinase and all other kinases, requires Mg (or Mn) for activity.
* Hexokinase is also one of the induced-fit model enzymes.
* It has two lobes that move towards each other when Glc is bound!
* Substrate-induced cleft closing is a general feature of kinases.
* Other kinases (Pyruvate kinase, phosphoglycerate kinase and PFK) also contain clefts between lobes that close when substrate is bound.

2. ISOMERIZATION OF G-6-P
3. PHOSPHORYLATION OF F-6-P
4. CLEAVAGE OF F-1,6BIP
5. ISOMERIZATION OF DIHYDROXYACETONE-P
6. OXIDATION OF GLYCERALDEHYDE 3-P.
Structure of glyceraldehyde 3-phosphate dehydrogenase
7: FORMATION OF ATP FROM 1,3-BIPGLYCERATE AND ADP
Q:Why does PEP have such a high P-ryl potential?
Pyruvate kinase deficiency:
Maintaining redox balances

Overview of carbohydrate metabolism.ppt

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21 April 2009

Bioactive Lipids: Membrane Sphingolipids And Gangliosides



Bioactive Lipids: Membrane Sphingolipids And Gangliosides
Powerpoint presentation by:Michael A. Collins, Ph.D.

Four major phospholipids in mammalian cell membranes
Structure of a ceramide (N-acylsphingosine)
Structure of sphingomyelin
Sphingosine

SPHINGOMYELIN-CERAMIDE-SPHINGOSINE BIOCHEMISTRY

Model of dynamics of membrane raft constituents and organization
Membrane raft-containing neutral and acid sphingomyelinases (SMase) activation and regulation in signal transduction
sphingomyelin
cerebrosides
and sulfatide(s)
Sphingolipidoses are lysosomal storage diseases with inherited defects in sphingolipid (SL) catabolism
Key points:
Structures of common sphingolipids
Sphingolipidoses are lysosomal storage diseases with inherited defects in sphingolipid (SL) catabolism: GANGLIOSIDOSES

Sphingolipids.ppt

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