Persius/hicric huggingface dataset:
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To revert a page to an earlier version:
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# Reverts and edit conflicts
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# Admin-only "rollback" link
On a user contributions page an admin has additional "rollback" links for contributions marked top (the last edit made by anybody to that article). The diff page showing the difference between an old and the current version of a page also has this link. Clicking on the link reverts to the last edit not made by the user being reverted. The feature is especially useful in the case of a known vandal, whose edits don't need to be checked before being reverted. An automatic edit summary Reverted edits by X to last version by Y is added. This feature cannot be used when the last two edits were by the same user, and one wants to revert to the previous version only.
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If the page has been created by the malicious user and nobody else has edited the page, clicking the rollback link gives the message Cannot revert edit; last contributor is only author of this article. In this case delete the page.
Rhinal cortex
The rhinal cortex is the cortex surrounding the rhinal fissure, including the entorhinal cortex and the perirhinal cortex.
It is a cortical region in the medial temporal lobe that is made up of Brodmann areas 28, 34, 35 and 36.
Input from all sensory cortexes flows to the perirhinal and parahippocampal cortexes, from where it continues to the entorhinal cortex, and proceeds to the hippocampus. After feedback from the hippocampus it then returns the same way back to the sensory cortexes.
Circuit diagram with the connections of the rhinal cortex

# Explicit memory
The rhinal cortex is proposed to be part of the neural circuit for explicit memory.
Studies comparing the results of selective lesions to the hippocampus and to the rhinal cortex, found that lesions to the hippocampus only did not cause impairment on object recognitions tests, but lesions to the rhinal cortex only, caused severe anterograde and retrograde impairments on object recognition tests. The conclusion was that object recognition (semantic memory) depends on the rhinal cortex.
Romana's sign

# Overview
Romana's sign, also known as a chagoma, is a medical term for the unilateral painless periorbital swelling associated with the acute stage of Chagas' disease. It is due to conjunctival swelling after contamination with the vector's feces, which contains the parasitic trypanosoma cruzi.
Although very characteristic of Chagas' disease, not all patients with the acute form develop Romana's sign.

# Etymology
It is named after Cecilio Romana, an Argentinian researcher who first described the phenomenon.
Roxithromycin

# Overview
Roxithromycin is a semi-synthetic macrolide antibiotic. It is used to treat respiratory tract, urinary and soft tissue infections. Roxithromycin is derived from erythromycin, containing the same 14-membered lactone ring. However, an N-oxime side chain is attached to the lactone ring.  It is also currently undergoing clinical trials for the treatment of male-pattern hair loss.
Roxithromycin is available under several brandnames, for example Surlid, Rulide, Biaxsig, Roxar and Roximycin.

# History
German pharmaceutical company Hoechst Uclaf brought out roxithromycin in 1987.

# Available forms
Roxithromycin is commonly available as tablets or oral suspension.

# Mechanism of action
Roxithromycin prevents bacteria from growing, by interfering with their protein synthesis. Roxithromycin binds to the subunit 50S of the bacterial ribosome, and thus inhibits the translocation of peptides. Roxithromycin has similar antimicrobial spectrum as erythromycin, but is more effective against certain gram-negative bacteria, particularly Legionella pneumophila.

# Pharmacokinetics
When taken before a meal, roxithromycin is very rapidly absorbed, and diffused into most tissues and phagocytes. Due to the high concentration in phagocytes, roxithromycin is actively transported to the site of infection. During active phagocytosis, large concentrations of roxithromycin are released.

# Metabolism
Only a small portion of roxithromycin is metabolised. Most of roxithromycin is secreted unchanged into the bile and some in expired air. Under 10% is excreted into the urine. Roxithromycin's half-life is 12 hours.

# Side effects
Most common side effects are gastrointestinal; diarrhoea, nausea, abdominal pain and vomiting.  Less common side effects include central or peripheral nervous system events such as headaches, dizziness, vertigo, and also the rarely seen rashes, abnormal liver function values and alteration in senses of smell and taste.

# Drug interactions
Roxithromycin has less interactions than erythromycin as it has a lower affinity for cytochrome P450.
Roxithromycin does not interact with hormonal contraceptives, prednisolone, carbamazepine, ranitidine or antacids.
When roxithromycin is administered with theophylline, some studies have shown an increase in the plasma concentration of theophylline. A change in dosage is usually not required but patients with high levels of theophylline at the start of the treatment should have their plasma levels monitored.
Roxithromycin appears to interact with warfarin. This is shown by an increase in prothrombin time (international normalised ratio (INR)) in patients taking roxithromycin and warfarin concurrently. As a consequence, severe bleeding episodes have occurred.
Saccharomyces

# Overview
Saccharomyces is a genus in the kingdom of fungi that includes many species of yeast.  Saccharomyces is from Latin meaning sugar fungi. Many members of this genus are considered very important in food production. One example is Saccharomyces cerevisiae, which is used in making wine, bread, and beer. Other members of this genus include Saccharomyces bayanus, used in making wine, and Saccharomyces boulardii, used in medicine.

# Morphology
Colonies of Saccharomyces grow rapidly and mature in 3 days. They are flat, smooth, moist, glistening or dull, and cream to tannish cream in color. The inability to utilize nitrate and ability to ferment various carbohydrates are typical characteristics of Saccharomyces.

## Cellular morphology
Blastoconidia (cell buds) are observed. They are unicellular, globose, and ellipsoid to elongate in shape. Multilateral (multipolar) budding is typical. Pseudohyphae, if present, are rudimentary. Hyphae are absent.
Saccharomyces produces ascospores, especially when grown on V-8 medium, acetate ascospor agar, or Gorodkowa medium. These ascospores are globose and located in asci. Each ascus contains 1-4 ascospores. Asci do not rupture at maturity. Ascospores are stained with Kinyoun stain and ascospore stain. When stained with Gram stain, ascospores are gram-negative while vegetative cells are gram-positive.

# History
The presence of yeast in beer was first suggested in 1680, although the genus was not named Saccharomyces until 1837. It was not until 1876 that Louis Pasteur demonstrated the involvement of living organisms in fermentation and in 1888, Hansen isolated brewing yeast and propagated leading to the importance of yeast in brewing. The use of microscopes for the study of yeast morphology and purity was crucial to understanding their functionality.

# Use in brewing
Brewing yeast are polyploid and belong to the Saccharomyces genera. The brewing strains can be classified into two groups; the ale strains (Saccharomyces cerevisiae, generally used for ale and stout) and the lager strains (Saccharomyces pastorianus or Saccharomyces uvarum). Lager strains are a hybrid strain of S. cerevisiae (ale strains) and S. bayanus (wine strains) and are often referred to as bottom fermenting. In contrast, ale strains are referred to as top fermenting strains, reflecting their separation characteristics in open square fermenters. Although the two species differ in a number of ways including their response to temperature, sugar transport and utilisation, the S. pastorianus and S. cerevisiae species are closely related within the Saccharomyces genus.
Saccharomyces yeasts can form symbiotic matrices with bacteria, and are used to produce kombucha, kefir and ginger beer.
Sacral nerves
The five sacral nerves emerge from the sacrum. Although the vertebral components of the sacrum are fused into a single bone, the sacral vertebrae are still used to number the sacral nerves.
- Posteriorly, they emerge from the posterior sacral foramina, and form the posterior branches of sacral nerves (including the medial clunial nerves).
- Anteriorly, they emerge from the anterior sacral foramina, and contribute to the sacral plexus (S1-S4) and coccygeal plexus.
Sacral plexus

# Overview
In human anatomy, the sacral plexus is a nerve plexus emerging from the sacral vertebrae (S1-S4), and which provides nerves for the pelvis and lower limbs.

# Structure
The sacral plexus is formed by::
- the lumbosacral trunk
- the anterior division of the first sacral nerve
- portions of the anterior divisions of the second and third sacral nerves
The nerves forming the sacral plexus converge toward the lower part of the greater sciatic foramen, and unite to form a flattened band, from the anterior and posterior surfaces of which several branches arise.
The band itself is continued as the sciatic nerve, which splits on the back of the thigh into the tibial nerve and common fibular nerve; these two nerves sometimes arise separately from the plexus, and in all cases their independence can be shown by dissection.
Often, the sacral plexus and the lumbar plexus are considered to be one large nerve plexus, the lumbosacral plexus.  The lumbosacral trunk connects  the two plexuses.

## Relations
The sacral plexus lies on the back of the pelvis between the piriformis muscle and the pelvic fascia. In front of it are the internal iliac artery, internal iliac vein, the ureter, and the sigmoid colon. The superior gluteal artery and vein run between the lumbosacral trunk and the first sacral nerve, and the inferior gluteal artery and vein between the second and third sacral nerves.
All the nerves entering the plexus, with the exception of the third sacral, split into ventral and dorsal divisions, and the nerves arising from these are as follows:

# Additional images
- Dissection of side wall of pelvis showing sacral and pudendal plexuses.
- The right sympathetic chain and its connections with the thoracic, abdominal, and pelvic plexuses.
Salpingectomy
Salpingectomy refers to the surgical removal of a Fallopian tube.

# Indications
The procedure was first performed by Lawson Tait in patients with a bleeding ectopic pregnancy; this procedure has since saved the lives of countless women. Other indications for a salpingectomy include infected tubes, (as in a hydrosalpinx) or as part of the surgical procedure for tubal cancer.

# Process
Salpingectomy has traditionally been done via a laparotomy; more recently however, laparoscopic salpingectomies have become more common as part of minimally invasive surgery.

# Related procedures
Salpingectomy is commonly done as part of a procedure called a salpingo-oophorectomy, where one or both ovaries, as well as one or both Fallopian tubes, are removed in one operation (a Bilateral Salpingo-Oophorectomy (BSO) if both ovaries and Fallopian tubes are removed).  If a BSO is combined with a hysterectomy, the procedure is commonly called a TAH-BSO: Total Abdominal Hysterectomy with a Bilateral Salpingo-Oophorectomy.
Salpingectomy is different from a salpingostomy, a procedure where an opening is made into the tube to remove the ectopic embryo, but the tube itself is not removed.

# History
Salpingectomies were performed in the United States in the 20th century in accordance with eugenics legislation. From Buck v. Bell:
The Virginia statute providing for the sexual sterilization of inmates of institutions supported by the State who shall be found to be afflicted with an hereditary form of insanity or imbecility, is within the power of the State under the Fourteenth Amendment.
Sandbox/00006

# FIRE: Focused Initial Rapid Evaluation
A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.
Boxes in salmon signify that an urgent management is needed.
Abbreviations: AVR: Aortic valve replacement; CCU:
Coronary care unit; CHF: Congestive cardiac failure;  CXR:  Chest X-ray; EKG: Electrocardiogram; MI: Myocardial infarction; OR: Operating room; TAVR: Transcatheter aortic valve replacement; TEE: Transesophageal echocardiogram; TTE: Transthoracic echocardiogram; HEENT: Head eye ear nose throat
-  "". External link in |title= (help).mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
-  "Predictors of complications in acute type B aortic dissection".
Sandbox/00025

# Pathogenesis
Several pathways are implicated in development of vascular remodeling in the pathogenesis of pulmonary hypertension
1. Thrombosis-mediated remodeling
Thrombin plays a key role in mediating vascular remodeling by activating platelet, upregulating angiogenesis-related genes (including tissue factor, basic fibroblast growth factor, and matrix metalloproteinase-2), and transactivating vascular endothelial growth factor by inducing the production of reactive oxygen species and the expression of the hypoxia inducible factor-1 alpha. Upregulation of tissue factor in the vasculature leads to initiation of coagulation cascade and migration and proliferation of smooth muscle cells upon vascular injury. In addition, platelet activation by thrombin results in the release of granules containing subtances that promote mitogenesis and vasoconstriction including VEGF, bFGF, platelet-derived growth factor, and serotonin, which also contribute to increased endothelial cell migration and proliferation.
2. Vasoconstriction-mediated remodeling
Imbalance of vasoactive signals is suggested in the pathogensis of remodeling. Reduced levels of vasodilatory mediators, in particular prostaglandin I2, nitric oxide, and cyclic guanine monophosphate, and elevated levels of vasocontricting molecules such as endothelin 1, thromboxane, and 5-hydroxytryptamine contribute to the alteration in the vascular tone. Downregulation of the voltage-gated potassium channels has also been linked with altered pulmonary vascular tone, dysregulation of cellular homeostasis, and induction of proliferative sequelae in vascular smooth muscle cells.
3. Proliferation-mediated remodeling
Serotonin exerts both vasoconstrictive and mitogenic effects on smooth muscle cells (SMC). Serotonin may bind to 5-hydroxytryptamine 1A and 2B receptors or may enter SMC via serotonin transporter which induces generation of reactive oxygen species, rho kinase, and mitogen-activated protein kinases. This in turn leads to thhe expression of growth factors and proliferation. Bone morphogenetic protein (BMP) is also involved in the SMC proliferation. Upon binding of BMP to the heterodimerized receptors, a group of cytoplasmic proteins known as receptor-mediated Smads are phosphorylated and translocated to the nucleus where they upregulate genes related to anti-proliferation. Serotonin is shown to antagonize the BMP/Smad pathway thus facilitating the proliferation of smooth muscle cells.
4. Inflammation-mediated remodeling
Influx of inflammatory effectors is stimulated by the release of chemokines such as CCL5 and CX3CL1. On the other hand, endothelial cell and smooth muscle cell dysfunction contributes to the release of vasomotor and growth mediators, activation of transcriptional factors, influx of calcium, and mitochondrial dysfunction. The net effect is a shift of balance in favor of proliferation and suppressed apoptosis, leading to remodeling of the pulmonary vasculature.
Sandbox/00032

# WHO Classification
Dengue case classification published by WHO in 2009 categorizes the disease into probable dengue or laboratory-confirmed dengue (with or without warning signs) and severe dengue (encompassing severe plasma leakage, severe bleeding, and severe organ involvement). The tables below describe the definitions of each category:

# Referemces
-  "Handbook for Clinical Management of dengue" (PDF)..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
-  "Dengue: guidelines for diagnosis, treatment, prevention and control" (PDF).
Sandbox/00035

# Overview
Acute lymphangitis may occur following direct inoculation of microorganisms through skin breaches or in the setting of erysipelas or cellulitis. Potential causative bacteria include Streptococcus pyogenes (most common), Staphylococcus aureus (if associated with prominent suppuration), Pasteurella multocida (if associated with animal bites), Erysipelothrix rhusiopathiae (if associated with handling of fish or raw meat), and Bacillus anthracis (if associated with exposure to infected animals or their products). Penicillins with or without anti-staphylococcal activity are the recommended initial treatment for acute lymphangitis.
Chronic granulomatous lymphangitis is typically caused by Sporothrix schenckii (rose gardener's disease) and treated with itraconazole. Sporotrichoid lesions may also result from infections with Mycobacterium marinum (swimming pool granuloma), Mycobacterium kansasii, Mycobacterium chelonae, Nocardia spp., Leishmania spp., Francisella tularensis, and Staphylococcus aureus (botryomycosis).
Filarial lymphangitis, most commonly caused by Wuchereria bancrofti (and sometimes by Brugia malayi or Brugia timori in Asia), is transmitted via mosquito bites and treated with diethylcarbamazine.
In addition to prompt antibiotics with appropriate coverage, adjunctive measures such as analgesics, anti-inflammatory drugs, limb elevation, or warm compresses may also be used for symptomatic relief.

# Principles of Therapy for Acute Lymphangitis Adapted from Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases.

## Mild to Moderate Disease
- Nontoxic patients may be managed in an outpatient setting with oral agents such as penicillin V or amoxicillin, with one preceding dose of intramuscular ceftriaxone for moderate cases.
- Pyogenic infection suggestive of a staphylococcal etiology should be treated with penicillinase-resistant beta-lactams (eg, dicloxacillin or cephalexin) in areas where methicillin-resistant Staphylococcus aureus (MRSA) is not prevalent.
- For empiric coverage of both MRSA and beta-hemolytic streptococci, oral antibiotic options include the following:
- Clindamycin alone
- Co-trimoxazole or doxycycline, in combination with a beta-lactam (eg, amoxicillin)
- Linezolid alone

## Severe Disease
- Hospitalization should be considered in the following conditions:
- Hypotension
- Marked left shift
- Elevated creatinine level
- Elevated creatine kinase level (23 times the upper limit of normal)
- C-reactive protein level >13 mg/L
- Low bicarbonate level
- If Staphylococcus aureus is suspected in patients with severe disease, empiric vancomycin should be administered parenterally.

# Antibiotic Therapy

# Adjunctive Therapy
- Chronic lymphedema may develop as a complication of recurrent lymphangitis. Remedies facilitating lymphatic drainage include manual massage, multilayered bandage wrapping, and intermittent pneumatic compression.