wikidoc - Recent changes [en]

I box gene transcriptions

2026-04-21T04:22:57Z

F box samplings

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	==F box samplings==		==F box samplings==
			[[I box gene transcriptions#F box samplings\|F box samplings]]

	As the F box is just the I box with a "T" in front of it. It does not occur because the I box does not occur!		As the F box is just the I box with a "T" in front of it. It does not occur because the I box does not occur!

Ethylene responsive element gene transcriptions

2026-04-21T03:18:36Z

ERE samplings

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	==ERE samplings==		==ERE samplings==
	{{main\|Model samplings}}		{{main\|Model samplings}}
			[[Ethylene responsive element gene transcriptions#ERE samplings\|ERE samplings]]

	Copying an apparent consensus sequence of ATTTCAAA and putting it in "⌘F" finds none located between ZSCAN22 and A1BG and one between ZNF497 and A1BG as can be found by the computer programs.		Copying an apparent consensus sequence of ATTTCAAA and putting it in "⌘F" finds none located between ZSCAN22 and A1BG and one between ZNF497 and A1BG as can be found by the computer programs.

Estrogen response element gene transcriptions

2026-04-21T01:24:49Z

ERE2 (Driscoll) samplings

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	==ERE (Matsumoto) samplings==		==ERE (Matsumoto) samplings==
			[[Estrogen response element gene transcriptions#ERE (Matsumoto) samplings\|ERE (Matsumoto) samplings]]

	Copying an abridged consensus sequence for the estrogen response element of AGGTTA (ci=TAACCT) and putting it in "⌘F" finds none located between ZSCAN22 and A1BG and none between ZNF497 and A1BG as can be found by the computer programs.		Copying an abridged consensus sequence for the estrogen response element of AGGTTA (ci=TAACCT) and putting it in "⌘F" finds none located between ZSCAN22 and A1BG and none between ZNF497 and A1BG as can be found by the computer programs.
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	==ERE (Yasar) samplings==		==ERE (Yasar) samplings==
			[[Estrogen response element gene transcriptions#ERE (Yasar) samplings\|ERE (Yasar) samplings]]

	Copying an abridged consensus sequence for the estrogen response element of GGTCAGGAT and putting it in "⌘F" finds none located between ZSCAN22 and A1BG and none between ZNF497 and A1BG as can be found by the computer programs.		Copying an abridged consensus sequence for the estrogen response element of GGTCAGGAT and putting it in "⌘F" finds none located between ZSCAN22 and A1BG and none between ZNF497 and A1BG as can be found by the computer programs.
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	==ERE1 (Driscoll) samplings==		==ERE1 (Driscoll) samplings==
			[[Estrogen response element gene transcriptions#ERE1 (Driscoll) samplings\|ERE1 (Driscoll) samplings]]

	Copying a responsive elements consensus sequence GGTCA and putting the sequence in "⌘F" finds five between ZNF497 and A1BG or six between ZSCAN22 and A1BG as can be found by the computer programs.		Copying a responsive elements consensus sequence GGTCA and putting the sequence in "⌘F" finds five between ZNF497 and A1BG or six between ZSCAN22 and A1BG as can be found by the computer programs.
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	==ERE2 (Driscoll) samplings==		==ERE2 (Driscoll) samplings==
			[[Estrogen response element gene transcriptions#ERE2 (Driscoll) samplings\|ERE2 (Driscoll) samplings]]

	Copying a responsive elements consensus sequence TGACC and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.		Copying a responsive elements consensus sequence TGACC and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.

Enhancer box gene transcriptions

2026-04-20T22:23:05Z

Enhancer box samplings

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 ==Enhancer box samplings==
 Regarding hypotheses 1:
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 The complement inverse is the same as the direct and the inverse is the same as the complement.
 ===Enhancer box (4560-2846) UTRs===

Hypertension in adolescents

2026-04-20T20:55:45Z

Show changes

Endosperm expression gene transcriptions

2026-04-20T18:45:33Z

Endosperm expression samplings

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	==Endosperm expression samplings==		==Endosperm expression samplings==
			[[Endosperm expression gene transcriptions#Endosperm expression samplings\|Endosperm expression samplings]]

	Copying an apparent consensus sequence of TGTGTCA and putting it in "⌘F" finds one located between ZSCAN22 and A1BG and none between ZNF497 and A1BG as can be found by the computer programs.		Copying an apparent consensus sequence of TGTGTCA and putting it in "⌘F" finds one located between ZSCAN22 and A1BG and none between ZNF497 and A1BG as can be found by the computer programs.

Endoplasmic reticulum stress response element gene transcriptions

2026-04-20T08:07:05Z

CCACG samplings

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	==CCACG samplings==		==CCACG samplings==
			[[Endoplasmic reticulum stress response element gene transcriptions#CCACG samplings\|CCACG samplings]]

	Copying an apparent consensus sequence of CCACG and putting it in "⌘F" finds eight located between ZSCAN22 and A1BG on the negative strand and none on the positive strand and six on the negative strand between ZNF497 and eight on the positive strand and A1BG as can be found by the computer programs.		Copying an apparent consensus sequence of CCACG and putting it in "⌘F" finds eight located between ZSCAN22 and A1BG on the negative strand and none on the positive strand and six on the negative strand between ZNF497 and eight on the positive strand and A1BG as can be found by the computer programs.

Hypertension in adolescents

2026-04-20T07:12:34Z

Show changes

Endoplasmic reticulum stress response element gene transcriptions

2026-04-20T06:25:56Z

CCAAT-N9-CCACG Samplings

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	==CCAAT-N9-CCACG Samplings==		==CCAAT-N9-CCACG Samplings==
			[[Endoplasmic reticulum stress response element gene transcriptions#CCAAT-N9-CCACG Samplings\|CCAAT-N9-CCACG Samplings]]

	According to So (2018) the endoplasmic reticulum stress response element should be CCAAT-N9-CCACG. Samplings below demonstrate that the ideal CCAAT-N9-CCACG or its complement inverse do not occur on either side of A1BG or close to ZSCAN22 or ZNF497.		According to So (2018) the endoplasmic reticulum stress response element should be CCAAT-N9-CCACG. Samplings below demonstrate that the ideal CCAAT-N9-CCACG or its complement inverse do not occur on either side of A1BG or close to ZSCAN22 or ZNF497.

EIN3 binding site gene transcriptions

2026-04-19T19:28:28Z

EIN3 analysis and results

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 ==EIN3 samplings==
 Copying a responsive elements consensus sequence ACGTACC and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.
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 # EIN3r8: ATGTACCT at 2781.
 # EIN3r6ci: AGGTTCGT at 1273.
 ==EIN3 analysis and results==

Hypertension in adolescents

2026-04-19T07:28:40Z

Show changes

EIF4E basal element gene transcriptions

2026-04-19T06:01:08Z

Samplings

← Older revision		Revision as of 06:01, 19 April 2026
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	==Samplings==		==Samplings==
			[[EIF4E basal element gene transcriptions#Samplings\|Samplings]]

	The '''EIF4E basal element''', also eIF4E, (4EBE) is a basal promoter element for the eukaryotic translation initiation factor 4E. "Interactions between 4EBE and upstream activator sites are position, distance, and sequence dependent."<ref name=Lynch/>		The '''EIF4E basal element''', also eIF4E, (4EBE) is a basal promoter element for the eukaryotic translation initiation factor 4E. "Interactions between 4EBE and upstream activator sites are position, distance, and sequence dependent."<ref name=Lynch/>

Congestive heart failure Management of Acute heart failure

2026-04-18T10:39:34Z

Transitional care plan: components (Class 1 recommendation):[2]

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	\|MedCond =Congestive heart failure\|Mannitol}}		\|MedCond =Congestive heart failure\|Mannitol}}

			=== '''Transitional care plan:''' ===

			* '''Structure of early post-discharge follow-up''':
			* It has two distinct events:<ref name=":3" />
			*# '''Follow-up phone call within 2-3 days of discharge'''
			*# '''Clinic visit within 7-14 days of hospital discharge'''
			* The first post-discharge appointment provides the opportunity to reassess clinical status, provide additional patient education, review medications and adjust doses, and address issues that might lead to readmission or worsening HF.

			==== '''Transitional care plan components''' (Class 1 recommendation):<ref name=":0" /> ====

			* Addressing any precipitating causes of worsening HF identified in the hospital

			* Adjusting diuretics based on volume status (including weight) and electrolytes
			* Coordination of safety laboratory checks (e.g., electrolytes after initiation or intensification of GDMT)
			* '''Plans for GDMT optimization''', including:
			** Plans for resuming medications held in the hospital
			** Plans for initiating new medications
			** '''Plans for titration of GDMT to goal doses as tolerated'''
			* Reinforcing HF education and assessing compliance with medical therapy and lifestyle modifications
			* Addressing high-risk characteristics (comorbid conditions, limitations in psychosocial support, impaired health literacy)
			* Referral to cardiac rehabilitation where appropriate
			* Referral to palliative care specialists in selected patients

	==References==		==References==

User:Nehal Eid

2026-04-18T10:30:11Z

← Older revision		Revision as of 10:30, 18 April 2026
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	'''Wikidoc contributions:'''		'''Wikidoc contributions:'''

			[[Intravenous drug use (recreational)]]

	[[Juvenile idiopathic arthritis]]		[[Juvenile idiopathic arthritis]]

	[[~~Sudden cardiac death~~]]		[[Hypertension and Blood Pressure Control in Diabetics]]

	[[~~Cosibelimab-ipdl~~]]		[[Lipid Management in Diabetics]]

	[[~~Olezarsen~~]]		[[Coronary heart disease in Diabetics]]

	[[~~Intravenous drug use (recreational)~~]]		[[Congestive heart failure Management of Acute heart failure]]

	[[~~Hypertension and Blood Pressure Control in Diabetics~~]]		[[Sudden cardiac death]]

	[[~~Lipid Management in Diabetics~~]]		[[Cosibelimab-ipdl]]

	[[~~Coronary heart disease in Diabetics~~]]		[[Olezarsen]]

Congestive heart failure Management of Acute heart failure

2026-04-18T10:28:06Z

Show changes

DREB box gene transcriptions

2026-04-18T06:00:13Z

DREB box sampling of A1BG promoters

← Older revision		Revision as of 06:00, 18 April 2026
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	==DREB box sampling of A1BG promoters==		==DREB box sampling of A1BG promoters==
			[[DREB box gene transcriptions#DREB box sampling of A1BG promoters\|DREB box sampling of A1BG promoters]]

	Consensus sequence for the dehydration-responsive element-binding (DREB) box is 3'-TACCGACAT-5'.		Consensus sequence for the dehydration-responsive element-binding (DREB) box is 3'-TACCGACAT-5'.

Advances in catheter based physical treatments

2026-04-16T16:09:32Z

@@ Line 1: / Line 1: @@
 __NOTOC__
-{{CMG}}
+{{CMG}} {{AE}} {{ACM}}
 ==Overview==
@@ Line 11: / Line 11: @@
 * developing ways of adequately binding the drugs to the stainless surface of the [[stent]] struts (the coating must stay bound despite marked handling and stent deformation stresses) and
 * developing coating controlled release mechanisms that release the drug slowly over about 30 days.
 ==References==

Rheumatoid arthritis overview

2026-04-16T12:40:15Z

Medical Therapy

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 ==Medical Therapy==
 The mainstay of treatment of [[rheumatoid arthritis]] is pharmacotherapy. Early diagnosis of [[rheumatoid arthritis]] is helpful in treatment. Choice of treatment depends on various factors such as stage of [[disease]], comorbid conditions, stage of therapy and presence of severe prognostic signs. There are two types of therapies- non-pharmacological therapy and pharmacological therapy. There are different drug regimen depending upon the stage of the disease. In active stage, combined therapy include disease-modifying antirheumatic drugs ([[DMARDs]]) are used along with the [[anti-inflammatory drugs]]. Therapy for resistant disease and flares is the addition of oral [[glucocorticoids]]. In case of the flare, add another [[DMARDs]] with [[methotrexate]] or replace with another [[DMARDs]].
 ==Surgical Therapy==

Acute lymphoblastic leukemia medical therapy

2026-04-16T12:02:57Z

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	{{Acute lymphoblastic leukemia}}		{{Acute lymphoblastic leukemia}}

	{{CMG}} {{shyam}} {{AE}} {{RT}} {{CLG}} {{ACM}}		{{CMG}} {{shyam}} {{AE}} {{RT}} {{CLG}} {{ACM}} {{MSD}}

	==Overview==		==Overview==

Coronary heart disease overview

2026-04-16T12:01:21Z

← Older revision		Revision as of 12:01, 16 April 2026
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	__NOTOC__		__NOTOC__
	{{Coronary heart disease}} {{CMG}}		{{Coronary heart disease}} {{CMG}} {{AE}} {{MSD}}

	==Overview==		==Overview==
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	==Treatment==		==Treatment==
	===Medical Therapy===		===Medical Therapy===
	Goals for treating coronary artery disease include lowering [[blood pressure]], ~~maintaining [[~~HbA1c~~]] levels to less than~~ 7%, and lowering [[LDL]] cholesterol. Long-term treatment will generally depend on the symptoms and severity of disease, and include [[aspirin]], [[ACE inhibitors]], and other ani-coagulant and anti-platelet regimens. The mainstay of treatment for [[chronic stable angina\|stable angina]] which occurs with exertion, includes [[nitroglycerin]]. When unstable angina causes symptoms at rest, or in the setting of an acute [[myocardial infarction]], the immediate therapy is [[morphine]], [[oxygen]], [[nitrate]] and [[aspirin]]. [[Angioplasty]] may also be required in cases of [[acute coronary syndrome]].		Goals for treating coronary artery disease include lowering [[blood pressure]], managing diabetes with cardiovascular-risk-reducing agents such as SGLT2 inhibitors and GLP-1 receptor agonists, independent of HbA1c target<ref name="pmid39289001">{{cite journal \|vauthors=Galli M, Gragnano F, Vrints C, Andreotti F \|title=2024 ESC guidelines on chronic coronary syndromes: what is new in pharmacotherapy? \|journal=Eur Heart J Cardiovasc Pharmacother \|volume=10 \|issue=7 \|pages=572–574 \|date=November 2024 \|pmid=39289001 \|doi=10.1093/ehjcvp/pvae069 \|url=}}</ref>, and lowering [[LDL]] cholesterol. Long-term treatment will generally depend on the symptoms and severity of disease, and include [[aspirin]], [[ACE inhibitors]], and other ani-coagulant and anti-platelet regimens.Low-dose colchicine (0.5 mg daily) should also be considered as an adjunctive anti-inflammatory therapy for long-term management. <ref name="pmid37558377">{{cite journal \|vauthors=Nelson K, Fuster V, Ridker PM \|title=Low-Dose Colchicine for Secondary Prevention of Coronary Artery Disease: JACC Review Topic of the Week \|journal=J Am Coll Cardiol \|volume=82 \|issue=7 \|pages=648–660 \|date=August 2023 \|pmid=37558377 \|doi=10.1016/j.jacc.2023.05.055 \|url=}}</ref> The mainstay of treatment for [[chronic stable angina\|stable angina]] which occurs with exertion, includes [[nitroglycerin]]. When unstable angina causes symptoms at rest, or in the setting of an acute [[myocardial infarction]], the immediate therapy is [[morphine]], supplemental oxygen (only if SpO₂ <90%), nitrate, and aspirin. [[Angioplasty]] may also be required in cases of [[acute coronary syndrome]].Beta-blockers should be used selectively: they are indicated when LVEF is <50%, or in the presence of angina, arrhythmias, or hypertension, but are no longer routinely recommended for all patients with chronic coronary disease.<ref name="pmid38766996">{{cite journal \|vauthors=Khorsandi M, Blumenthal RS, Blaha MJ, Kohli P \|title=The ABCs of the 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA guideline for the management of patients with chronic coronary disease \|journal=Clin Cardiol \|volume=47 \|issue=5 \|pages=e24284 \|date=May 2024 \|pmid=38766996 \|pmc=11103637 \|doi=10.1002/clc.24284 \|url=}}</ref>

	===Primary Prevention===		===Primary Prevention===
	The [[LDL]] target in primary prevention depends upon the patient's [[risk factors]]. If the ~~patient has CHD or its equivalent~~, ~~then the LDL goal is under 100 mg~~/dl. ~~If the patient has 2~~ risk ~~factors~~, the LDL ~~goal is 130 mg~~/dl. ~~If the patient has~~ < ~~2 risk factors~~, ~~the LDL goal~~ is < ~~160 mg~~/dl. Attempts should be made to reduce [[triglyceride]] levels and to increase [[HDL]] levels. The underlying causes for existing [[dyslipidemia]]s should be identified and appropriately managed. Drugs that cause dyslipidemias should be avoided. Patients should be evaluated reguarly for the presence of risk factors for coronary heart disease, and those with increased risk should be counseled on the beneficial effects of daily [[aspirin]] therapy. Patients should also regularly be counseled about modifying risk factors such as [[obesity]], [[hypertension]], [[smoking]], and the benefits of an [[exercise]] plan.		The [[LDL]] target in primary prevention depends upon the patient's [[risk factors]]. LDL targets in primary prevention should be guided by estimated 10-year ASCVD risk using the PREVENT™ equations<ref name="urlACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology">{{cite web \|url=https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia \|title=ACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology \|format= \|work= \|accessdate=}}</ref>. Statin therapy is recommended for those with intermediate risk (5–<10%) and reasonable for those with borderline risk (3–<5%) after shared decision-making, with the goal of achieving at least a 50% LDL-C reduction from baseline<ref name="urlACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology">{{cite web \|url=https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia \|title=ACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology \|format= \|work= \|accessdate=}}</ref>.Non-statin therapies — including ezetimibe, bempedoic acid, and PCSK9 inhibitors should be considered when statin therapy alone is insufficient.<ref name="urlACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology">{{cite web \|url=https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia \|title=ACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology \|format= \|work= \|accessdate=}}</ref> Attempts should be made to reduce [[triglyceride]] levels and to increase [[HDL]] levels.Coronary artery calcium (CAC) scoring and Lp(a) measurement should be considered to further refine cardiovascular risk and guide treatment intensity.<ref name="urlACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology">{{cite web \|url=https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia \|title=ACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology \|format= \|work= \|accessdate=}}</ref> The underlying causes for existing [[dyslipidemia]]s should be identified and appropriately managed. Drugs that cause dyslipidemias should be avoided. Patients should be evaluated reguarly for the presence of risk factors for coronary heart disease, and those with increased risk should be counseled on the beneficial effects of daily [[aspirin]] therapy. Patients should also regularly be counseled about modifying risk factors such as [[obesity]], [[hypertension]], [[smoking]], and the benefits of an [[exercise]] plan.

	===Secondary Prevention===		===Secondary Prevention===
	Patients who should be treated with secondary prevention are those with established atherosclerosis including peripheral artery		Patients who should be treated with secondary prevention are those with established atherosclerosis including peripheral artery disease; carotid artery disease; atherosclerotic aortic disease; diabetes and those with a 10-year ASCVD risk >20% by contemporary risk calculators (e.g., PREVENT™ equations or SCORE2).<ref name="url2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines \| Circulation">{{cite web \|url=https://www.ahajournals.org/doi/10.1161/CIR.0000000000001423 \|title=2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines \| Circulation \|format= \|work= \|accessdate=}}</ref> There are 13 aspects of secondary prevention: Smoking cessation; blood pressure control; lipid-lowering; increasing physical activity; weight loss; diabetes control; antiplatelet agents/anticoagulants; RAS blockers; beta-blockers; depression management; cardiac rehabilitation, influenza vaccine and low-dose colchicine (0.5 mg/day) for anti-inflammatory residual risk reduction.<ref>SEC Working Group for the 2024 ESC guidelines for the management of chronic coronary syndromes and SEC Guidelines Committee. (2025). Comments on the ESC 2024 guidelines for the management of chronic coronary syndromes. ''Revista Espanola de Cardiologia (English Ed.)'', ''78''(3), 170–175. <nowiki>https://doi.org/10.1016/j.rec.2024.10.007</nowiki></ref> Please note that secondary prevention guidelines, especially, those involving medication, may differ between [[Unstable Angina\|UA/NSTEMI]]; [[STEMI]]; and [[Chronic Stable Angina]].
	disease; carotid artery disease; atherosclerotic aortic disease; diabetes and those with a ~~Framingham Risk Score of~~ > 20%.
	There are 12 aspects of secondary prevention: Smoking cessation; blood pressure control; lipid-lowering; increasing physical activity; weight loss; diabetes control; antiplatelet agents/anticoagulants; RAS blockers; beta-blockers; depression management; cardiac rehabilitation ~~and~~ influenza vaccine. Please note that secondary prevention guidelines, especially, those involving medication, may differ between [[Unstable Angina\|UA/NSTEMI]]; [[STEMI]]; and [[Chronic Stable Angina]].

	==References==		==References==

Downstream TFIIB recognition element gene transcriptions

2026-04-16T07:20:49Z

dBRE samplings

← Older revision		Revision as of 07:20, 16 April 2026
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	27. CACCAAA IDC 1 (4063)		27. CACCAAA IDC 1 (4063)
	28. CACCAAC 0		28. CACCAAC 0
	29. (1) pp -40 CACCCCA -34 (1) np +29 ~~GTGGGGT~~ +35 ± 50 2 IDC 1 (7070)		29. (1) pp -40 CACCCCA -34 (1) np +29 CACCCCA +35 ± 50 2 IDC 1 (7070)
	30. CACCCCC IDC 4 (3590NM) (7070) (57611) (57715)		30. CACCCCC IDC 4 (3590NM) (7070) (57611) (57715)
	31. CACCCAA 0		31. CACCCAA 0

Sandbox

2026-04-16T00:52:30Z

← Older revision		Revision as of 00:52, 16 April 2026
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			== ACS Treatment ==
			Primary Prevention:

	~~{{familytree/start}}~~		'''Equivalent intensity for CHD-risk equivalents (LoE: A):''' Patients with established CHD should be targeted for secondary prevention. Crucially, patients with a '''CHD risk equivalent''' — defined as atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or a Framingham-calculated 10-year risk exceeding 20% — should receive '''the same intensity of risk factor intervention''' as those with overt, clinically apparent CHD.
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| A01 \| \| \| \| \| \|A01=Adult ALL }}~~
	~~{{familytree \| \|,\|-\|-\|-\|v\|-\|-\|-\|-\|-\|-\|+\|-\|-\|-\|-\|-\|-\|-\|-\|-\|.\| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| D01 \| \| D02 \| \| \| \| \| D03 \| \| \| \| \| \| \| \| D05 \| \| \| \|D01=Burkitt Leukemia\|D02=PH-Positive B-ALL\|D03=PH-negative B-ALL\|D05=T-ALL}}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|,\|-\|-\|^\|-\|-\|.\| \| \| \|,\|-\|-\|^\|-\|-\|.\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	{{familytree \| E01 \| \| E02 \| \| E03 \| \| \| \| E04 \| \| E05 \| \| \| \| E06 \| \| \|E01=R-hyper CVAD<br> DA-R-EPOCH\|E02=Chemotherapt+TKI <br> Blinatumomab+TKI\|E03=Younger adults\|E04=Older Adults\|E05=ETP\|E06=Non ETP}}
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \|}}~~
	{{familytree \| \|!\| \| \| \|!\| \| \| F01 \| \| \| \| F02 \| \| F03 \| \| \| \| F04 \| \|F01=Chemotherapy+<br>blinatumomab\|F02=Chemotherapy+<br>blinatumumab+InO <br>Chemotherapy-free blinatumomab + InO\|F03=Chemotherapy+pegAsp+<br>nelarabine+venetoclax\|F04=Chemotherapy+pegAsp+<br>nelarabine}}
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|`\|-\|-\|-\|^\|-\|-\|-\|^\|-\|-\|v\|-\|-\|^\|-\|-\|-\|^\|-\|-\|-\|-\|-\|~~'~~\| \| \| }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| G01 \| \| \| \| \| \| \| \| \| \| \| \| \| \|G01=<div style="float: left; text~~-~~align~~: ~~left; height~~: ~~3em; width: 20em;">~~ '''~~Measurable residual disease monitoring~~'''~~<br> </div>}} }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \| \| \| \| \| }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| H01 \| \| \| \| \| \| \| \| \| \| \| \| \| \| \|H01=<div style="float: left; text~~-~~align: left;">~~'''~~Alloegenic hematopoietic stem cell transplant~~''' ~~<br>•Ph-like ALL~~ with ~~CRLF2 and JAK vairants<br>•High-risk cytogenetics in B-ALL<br>•High-risk Ph-positive B-ALL: IZKF1 genotype<br>•T-ALL: ETP-ALL<br>•Persistent measurable residual disease by NGS<br> </div>}}~~
	~~{{familytree/end}}~~

User:Hasnain Ali

2026-04-14T19:59:22Z

Recently Edited Topics

← Older revision		Revision as of 19:59, 14 April 2026
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	I create original content on my areas of interest and refresh older chapters to keep the medical information current.		I create original content on my areas of interest and refresh older chapters to keep the medical information current.

	* Medical Officer with Dept. of Neurology, Liaquat University hospital Hyderabad/Jamshoro, Pakistan.		* Resident Medical Officer with Dept. of Neurology, Liaquat University hospital Hyderabad/Jamshoro, Pakistan.

	I provide inpatient and outpatient neurological care, managing up to 5 inpatients daily and around 30 clinic and emergency patients per week. Alongside clinical duties, I participated in multidisciplinary academic activities and contributed to research through systematic data collection and documentation.		I provide inpatient and outpatient neurological care, managing up to 5 inpatients daily and around 30 clinic and emergency patients per week. Alongside clinical duties, I participated in multidisciplinary academic activities and contributed to research through systematic data collection and documentation.
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	*'''Dr. Ruth. K. M. Pfau Civil hospital Karachi, Pakistan (July/2021 - Jan/2022)'''<br>'''Position:''' Intern/House officer<br>'''Supervisor Attending:''' Multiple		*'''Dr. Ruth. K. M. Pfau Civil hospital Karachi, Pakistan (July/2021 - Jan/2022)'''<br>'''Position:''' Intern/House officer<br>'''Supervisor Attending:''' Multiple

			==Recently Edited Topics==
			* [[Transient global amnesia\|Transient Global Amnesia]]

Low back pain conservative management

2026-04-14T16:24:46Z

Physical Therapy

← Older revision		Revision as of 16:24, 14 April 2026
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	The Mckenzie Method has been shown to be a modestly effective therapy for adults with chronic low back pain. A 2011 summary of 4 studies showed consistent significant improvement in pain and function although only one study had a large enough population to demonstrate effect sizes on pain and functional outcomes, 0.50 and 0.39 respectively.<ref name="pmid22135496">{{cite journal\| author=Dunsford A, Kumar S, Clarke S\| title=Integrating evidence into practice: use of McKenzie-based treatment for mechanical low back pain. \| journal=J Multidiscip Healthc \| year= 2011 \| volume= 4 \| issue= \| pages= 393-402 \| pmid=22135496 \| doi=10.2147/JMDH.S24733 \| pmc=PMC3215349 \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22135496 }} </ref>		The Mckenzie Method has been shown to be a modestly effective therapy for adults with chronic low back pain. A 2011 summary of 4 studies showed consistent significant improvement in pain and function although only one study had a large enough population to demonstrate effect sizes on pain and functional outcomes, 0.50 and 0.39 respectively.<ref name="pmid22135496">{{cite journal\| author=Dunsford A, Kumar S, Clarke S\| title=Integrating evidence into practice: use of McKenzie-based treatment for mechanical low back pain. \| journal=J Multidiscip Healthc \| year= 2011 \| volume= 4 \| issue= \| pages= 393-402 \| pmid=22135496 \| doi=10.2147/JMDH.S24733 \| pmc=PMC3215349 \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22135496 }} </ref>

	A randomized controlled ~~trail~~ in 2015 found minimal benefit.<ref name="v851">{{cite journal \| last1=Fritz \| first1=Julie M. \| last2=Magel \| first2=John S. \| last3=McFadden \| first3=Molly \| last4=Asche \| first4=Carl \| last5=Thackeray \| first5=Anne \| last6=Meier \| first6=Whitney \| last7=Brennan \| first7=Gerard \| title=Early Physical Therapy vs Usual Care in Patients With Recent-Onset Low Back Pain: A Randomized Clinical Trial \| journal=JAMA \| volume=314 \| issue=14 \| date=2015-10-13 \| issn=0098-7484 \| doi=10.1001/jama.2015.11648 \| page=1459 \| url=http://jama.jamanetwork.com/article.aspx?doi=10.1001/jama.2015.11648 \| access-date=2026-04-12}}</ref>		A [[randomized controlled trial]] in 2015 found minimal benefit.<ref name="v851">{{cite journal \| last1=Fritz \| first1=Julie M. \| last2=Magel \| first2=John S. \| last3=McFadden \| first3=Molly \| last4=Asche \| first4=Carl \| last5=Thackeray \| first5=Anne \| last6=Meier \| first6=Whitney \| last7=Brennan \| first7=Gerard \| title=Early Physical Therapy vs Usual Care in Patients With Recent-Onset Low Back Pain: A Randomized Clinical Trial \| journal=JAMA \| volume=314 \| issue=14 \| date=2015-10-13 \| issn=0098-7484 \| doi=10.1001/jama.2015.11648 \| pmid = 26461996 \| page=1459 \| url=http://jama.jamanetwork.com/article.aspx?doi=10.1001/jama.2015.11648 \| access-date=2026-04-12}}</ref> Outcomes were measured with the Oswestry Disability Index (ODI: range 0 to 100) which has a recommended minimum clinically important difference (MCID) of 6<ref name="pmid11175676">{{cite journal \| last1=Fritz \| first1=J. M. \| last2=Irrgang \| first2=J. J. \| title=A comparison of a modified Oswestry Low Back Pain Disability Questionnaire and the Quebec Back Pain Disability Scale \| journal=Physical Therapy \| volume=81 \| issue=2 \| date=2001 \| issn=0031-9023 \| pmid=11175676 \| doi=10.1093/ptj/81.2.776 \| pages=776–788 \| url=https://pubmed.gov/11175676 \| access-date=2026-04-14}}</ref>. While both the intervention and usual care group had improvement well above the MCID, the "Mean Difference Between Groups in Change from Baseline" were less than 4 at all time points.

	===Pilates===		===Pilates===

← Older revision		Revision as of 00:52, 16 April 2026
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			== ACS Treatment ==
			Primary Prevention:

	~~{{familytree/start}}~~		'''Equivalent intensity for CHD-risk equivalents (LoE: A):''' Patients with established CHD should be targeted for secondary prevention. Crucially, patients with a '''CHD risk equivalent''' — defined as atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or a Framingham-calculated 10-year risk exceeding 20% — should receive '''the same intensity of risk factor intervention''' as those with overt, clinically apparent CHD.
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| A01 \| \| \| \| \| \|A01=Adult ALL }}~~
	~~{{familytree \| \|,\|-\|-\|-\|v\|-\|-\|-\|-\|-\|-\|+\|-\|-\|-\|-\|-\|-\|-\|-\|-\|.\| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| D01 \| \| D02 \| \| \| \| \| D03 \| \| \| \| \| \| \| \| D05 \| \| \| \|D01=Burkitt Leukemia\|D02=PH-Positive B-ALL\|D03=PH-negative B-ALL\|D05=T-ALL}}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|,\|-\|-\|^\|-\|-\|.\| \| \| \|,\|-\|-\|^\|-\|-\|.\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	{{familytree \| E01 \| \| E02 \| \| E03 \| \| \| \| E04 \| \| E05 \| \| \| \| E06 \| \| \|E01=R-hyper CVAD<br> DA-R-EPOCH\|E02=Chemotherapt+TKI <br> Blinatumomab+TKI\|E03=Younger adults\|E04=Older Adults\|E05=ETP\|E06=Non ETP}}
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \|}}~~
	{{familytree \| \|!\| \| \| \|!\| \| \| F01 \| \| \| \| F02 \| \| F03 \| \| \| \| F04 \| \|F01=Chemotherapy+<br>blinatumomab\|F02=Chemotherapy+<br>blinatumumab+InO <br>Chemotherapy-free blinatumomab + InO\|F03=Chemotherapy+pegAsp+<br>nelarabine+venetoclax\|F04=Chemotherapy+pegAsp+<br>nelarabine}}
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|`\|-\|-\|-\|^\|-\|-\|-\|^\|-\|-\|v\|-\|-\|^\|-\|-\|-\|^\|-\|-\|-\|-\|-\|~~'~~\| \| \| }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| G01 \| \| \| \| \| \| \| \| \| \| \| \| \| \|G01=<div style="float: left; text~~-~~align~~: ~~left; height~~: ~~3em; width: 20em;">~~ '''~~Measurable residual disease monitoring~~'''~~<br> </div>}} }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \| \| \| \| \| }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| H01 \| \| \| \| \| \| \| \| \| \| \| \| \| \| \|H01=<div style="float: left; text~~-~~align: left;">~~'''~~Alloegenic hematopoietic stem cell transplant~~''' ~~<br>•Ph-like ALL~~ with ~~CRLF2 and JAK vairants<br>•High-risk cytogenetics in B-ALL<br>•High-risk Ph-positive B-ALL: IZKF1 genotype<br>•T-ALL: ETP-ALL<br>•Persistent measurable residual disease by NGS<br> </div>}}~~
	~~{{familytree/end}}~~