12.3.17
When your teacher said they’re going to post a study guide but they don’t qq
Music mood: Rubber Human - Mili
Simplified version of Dopamine’s dose-dependent MAJOR effects:
low doses - activates D1 receptors (Gs) - vasodilates renal blood vessels*
med.doses - activates B1 receptors (Gs) - increases heart rate/contractility etc..
high doses - activates A1 (Gq) - vasoconstricts,
*increased renal perfusion, GFR, also vasodilates mesenteric and coronary vessels
source: http://reference.medscape.com/drug/intropin-dopamine-342435
Hi optom! I'm very new to the studyblr community and it's my first term of university. I was a straight A student in high school and i am not performing well in my classes. In fact... I'm doing terribly. About a B to B- average. I know I'm probably not the first to go through so I've been trying to find posts that help students cope with this. Resources. Helpful tips. Is there a tag you can recommend? Any posts that you've encountered/wrote that I could peruse? Thank you very much for any help!
Hey there, thanks for asking. This is actually a very common problem experienced by people as they progress from high school to university.
The problem is that mediocre study techniques and a combination of natural ability may have gotten you straight As whilst in high school, but it’s just not going to cut it in university. Cracking down on yourself and sitting down for more hours isn’t going to make your grades much better; it’s just doing more of the same mediocre studying.
So you basically need to read up on good studying techniques and actually apply them to your studies.
I actually have a web directory of all my study tips which already lists all these links.
So because the problem you have at its base is most likely that you’re using high school level techniques to tackle university-level problems, you’ll need to find resources on all areas related to good studying. For some of these areas, I have a related post, but for the more generalised topics like procrastination, I haven’t yet put one out because if I do, I want to be certain that the post will be unique, useful and practical.
Without further ado, here’s a list of all the tags/areas you should work through and evaluate whether you need to change your current study habits if you want to be a 4.0/HD student at university.
Firstly, have a read of my recent answer about 20 Things You Can Do To Prepare for University, and click through to any of the parts of my 15-Part University 101 Series.
Time management
Organisation (see Part 3 Studying and Part 8 Four Secrets from University and Part 11 Adapting to Uni Studying which covers how you can manage university workloads on the whole and specific changes to your studies you should make)
Motivation
Discipline / Staying Focused
Procrastination (see post by @samsstudygram)
Study Methods (I’ve got one on the Blank Paper Method and the Cornell Method)
Exams (I’ve got a multi-part series in the works)
Study Materials (see Part 2 of my University Series for some tips)
Studying from Textbooks (see Part 12 How To Study From Textbooks in Uni which deals with this specifically)
Self Care (you can see my tag here of my own + useful curated posts)
Spaced Repetition (use Anki!)
Study Space (I have a masterpost with tips here)
Hope that helps! If you have a specific question about any areas then let me know!
Pizza heaven! Quick and easy! Recipe up on blog: www.studydiaryofamedstudent.wordpress.com
11.19.17
2 more days until break
Music mood: Mili - Miracle Milk
Eukaryotes of microbiology
[17 Dec 2017] (i thought i’d posted but it’s not appearing? ):) so sorry for the lack of original posts all these months! school has been so tough & i’ve just completed my mid-sem assessments & it’s finally my break! can’t wait to unwind and catch up on my sleep ;-;
Schematic of gram positive diplococci (Streptococcus pneumoniae): Note that the diplococci are lancet shaped
First line of defence + first to act
A primitive response (exists in animals and some plants)
Non-specialised and without ‘memory’
Consists of:
Physical barriers (eg skin and mucosa//tight junctions, airflow)
Chemical barriers (eg enzymes, lung surfactant, antimicrobals)
Soluble mediators of inflammation (eg cytokines)
Microbal defence (eg commensal competition, secreted antimicrobals)
Cells (eg phagocytes)
Receptors to recognise presence of pathogen/injury - results in inflammation
Complement Proteins
liver-derived
circulate in serum in inactive form
activated by pathogens during innate response
functions include lysis, chemotaxis and opsonisation
Auxiliary Cells
Mediate inflammation as part of the immune response. The main auxiliary cells involved in the immune response are Basophils, Mast cells and Platelets.
Basophils
Leukocyte containing granules
on degranulation release histamine + platelet activating factor
causing increased vascular permeability and smooth muscle contraction
also synthesise and secrete other mediators that control the development of immune system reactions
Mast Cells
Also contain granules
However they are not circulating cells - found close to blood vessels in all types of tissue especially mucosal and epithelial tissues.
rapidly release inflammatory histamine but this is IgE dependant so not innate
Platelets
normally function in blood clotting
also release inflammatory mediators
Cytokines and chemokines
Produced by many cells but especially mØ (macrophages), initiate inflammatory response and act on blood vessels
interferons - antiviral protection
chemokines - recruit cells
interleukines - fever inducing, IL-6 induces acute phase proteins
IL-1 - encourages leukocytes to migrate to infected/damaged tissue
as does tumour necrosis factor (TNFa)
Acute phase proteins
Liver derived proteins
plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation
called the acute-phase reaction
triggered by inflammatory cytokines ( IL-1, IL-6, TNFα)
help mediate inflammation ( fever, leukocytosis, increased cortisol, decreased thyroxine, decreased serum iron, etc)
activate complement opsonisation
Inflammation
Cytotoxic Cells
Eosinophils/natural killer cells, cytotoxic T cells
kill target via release of toxic granules
dendritic cell derived IL-12 helps activate NK cells
Phagocytes
mono-nuclear = long-lived; polynuclear = short-lived
engulf, internalize and destroy
phagosome forms around microbe
enzyme filled with lysosomes fuses to form phagolysosome
organism is digested
fragments are either ‘presented’ or exocytosed
phagocytosis requires recognition of microbe via receptors for
PAMPs (pathogen associated molecular patterns - eg flagella or capsule) - recognised by toll-like receptors
activated complement
antibody
The innate immune response primes for the adaptive
B-cells are primed by activated complement
Th1 cell differentiation needs pro-inflammatory cytokines
Slime mould