Persius/hicric huggingface dataset:
Cutaneous lymphoid cutis

# Overview
Cutaneous lymphoid hyperplasia (also known as "borrelial lymphocytoma," "Lymphadenosis benigna cutis," "Lymphocytoma cutis," "Pseudolymphoma," "Pseudolymphoma of Spiegler and Fendt," "Sarcoidosis of Spiegler and Fendt," "SpieglerFendt lymphoid hyperplasia," and "SpieglerFendt sarcoid") refers to a groups of benign cutaneous disorders characterized by collections of lymphocytes, macrophages, and dendritic cells in the skin.:725  Conditions included in this groups are::725
- Cutaneous lymphoid hyperplasia with nodular pattern, a condition of the skin characterized by a solitary or localized cluster of asymptomatic erythematous to violaceous papules or nodules.:725
- Cutaneous lymphoid hyperplasia with bandlike and perivascular patterns, a condition of the skin characterized by skin lesions that clinically resemble mycosis fungoides.:726
- Jessner lymphocytic infiltrate of the skin (also known as "Benign lymphocytic infiltration of the skin," "Jessner lymphocytic infiltration of the skin," "JessnerKanof lymphocytic infiltration of the skin," and "Lymphocytic infiltrate of Jessner") is a cutaneous condition characterized by a persistent papular and plaque-like skin eruption which can occur on the neck, face and back and may re-occur. This is an uncommon skin disease and is a benign collection of lymph cells. The cause of this is not known and can be hereditary.:1887:727 It is named for Max Jessner. It has been suggested that it is equivalent to lupus erythematosus tumidus.

# Diagnosis

## Physical Examination

### Skin
- Lymphocytoma cutis. Adapted from Dermatology Atlas.
- Lymphocytoma cutis. Adapted from Dermatology Atlas.
- Lymphocytoma cutis. Adapted from Dermatology Atlas.
- Lymphocytoma cutis. Adapted from Dermatology Atlas.
- Lymphocytoma cutis. Adapted from Dermatology Atlas.
- Lymphocytoma cutis. Adapted from Dermatology Atlas.
- Lymphocytoma cutis. Adapted from Dermatology Atlas.
- Lymphocytoma cutis. Adapted from Dermatology Atlas.
DAZ associated protein 1
DAZ-associated protein 1 is a protein that in humans is encoded by the DAZAP1 gene.

# Function
In mammals, the Y chromosome directs the development of the testes and plays an important role in spermatogenesis. A high percentage of infertile men have deletions that map to regions of the Y chromosome. The DAZ1 (Deleted in Azoospermia) gene cluster maps to the AZFc region of the Y chromosome and is deleted in many azoospermic and severely oligospermic men. It is thought that the DAZ gene cluster arose from the transposition, amplification, and pruning of the ancestral autosomal gene DAZL also involved in germ cell development and gametogenesis. This gene encodes an RNA-binding protein with two RNP motifs that was originally identified by its interaction with the infertility factors DAZ and DAZL. Two isoforms are encoded by transcript variants of this gene.

# Interactions
DAZ associated protein 1 has been shown to interact with DAZ1.
Hypertrophy of the heart

# Differential Diagnosis of Causes of Hypertrophy
(In alphabetical order, not by frequency) 

## Left Atrial Enlargement
- Atrial aneurysm
- Infective endocarditis
- Left heart failure
- Mitral regurgitation
- Mitral stenosis
- Mitral valve prolapse
- Myxedema
- Patent Ductus Arteriosus
- Ventricular septal defect

## Left Ventricular Hypertrophy
- Acromegaly
- Alcoholic cardiomyopathy
- Aortic coarctation
- Aortic regurgitation
- Aortic stenosis
- Chronic Renal Failure
- Familial dilated and hypertrophic cardiomyopathy
- Hypertrophic cardiomyopathy (HCM)
- Idiopathic dilated cardiomyopathy
- Mitral regurgitation
- Patent Ductus Arteriosus
- Restrictive cardiomyopathy
- Thalassemia

## Right Atrial Enlargement
- Atrial aneurysm
- Atrial septal defect
- Ebstein's anomaly
- Pulmonic stenosis
- Right heart failure
- Tricuspid prolapse
- Tricuspid regurgitation
- Tricuspid stenosis
- Tumor

## Right Ventricular Hypertrophy
- Atrial septal defect
- Chronic Obstructive Pulmonary Disease (COPD)
- Cor pulmonale
- Eisenmenger's Syndrome
- Left ventricular hypertrophy or Left ventricular dilation
- Mitral stenosis
- Pickwickian Syndrome
- Pulmonic regurgitation
- Pulmonic stenosis
- Tetralogy of Fallot
- Transposition of the Great Vessels
- Tricuspid regurgitation
- Ventricular septal defect

# Pathological Findings
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission.  PEIR, University of Alabama at Birmingham, Department of Pathology
- Biventricular Hypertrophy
- Biventricular Hypertrophy
- Gross excellent example of concentric left ventricular hypertrophy
- Left Ventricular Hypertrophy: Gross natural color anterior view intact heart showing disproportionate size of left ventricle by its inferior extent much below the right ventricle apex (quite good example)
- Myocardial Infarct: Gross natural color apical section showing large left ventricle infarct and right ventricular hypertrophy
- Right ventricular hypertrophy
Restrictive lung disease

# Overview
Restrictive lung disease (RLD) is a group of diseases characterized by an inability to attain complete expansion of the lungs. This may result from an abnormality in the parenchyma of the lungs or an abnormality outside the lung parenchyma (such as fluid accumulation or musculoskeletal abnormalities) hindering normal lung expansion and thus ability to ventilate normally. Restrictive lung diseases presents with a restrictive pattern on pulmonary function test and includes a decrease in total lung capacity (TLC), residual volume (RV), forced vital capacity (FVC), forced expiatory volume (FEV1), and a normal to increased FEV1/FVC ratio. Unlike obstructive lung disease (characterized by air trapping within the lungs), restrictive lung diseases result in decreased lung volumes and a lower than normal amount of air within the lungs. RLDs include acute respiratory distress syndrome, hypersensitivity pneumonitis, occupational lung diseases, pleural effusion, interstitial lung disease, sarcoidosis, and neuromuscular diseases such as scoliosis, muscular dystrophy, amyotropic lateral sclerosis (ALS), and myasthenia gravis.

# Classification
Various diseases that present with a restrictive pattern on pulmonary function tests include:
- Acute respiratory distress syndrome
- Hypersensitivity pneumonitis
- Occupational lung diseases
- Pleural Effusion
- Interstitial lung disease
- Sarcoidosis
- Neuromuscular diseases
Scoliosis
Muscular dystrophy
Amyotropic lateral sclerosis (ALS)
Myasthenia gravis
- Scoliosis
- Muscular dystrophy
- Amyotropic lateral sclerosis (ALS)
- Myasthenia gravis

# Spirometry Findings in Various Lung Conditions
Spirometry can help distinguish restrictive lung disease from obstructive lung diseases. On spirometry the findings include:

# Approach to Lung Disorders

# Differentiating Restrictive Lung Disease from other Diseases
Restrictive lung disease must be differentiated from other diseases that cause dyspnea, cough, hemoptysis, and fever such as ARDS, hypersensitivity pneumonitis, pneumoconiosis, sarcoidosis, pleural effusion, interstitial lung disease (ILD), lymphocytic interstitial pneumonia, obesity, pulmonary eosinophilia, and neuromuscular disorders.
Deep parotid lymph nodes
The deep parotid lymph nodes are lymph nodes found below the parotid gland.
The afferents of the subparotid glands drain the nasal part of the pharynx and the posterior parts of the nasal cavities.
Their efferents pass to the superior deep cervical glands.

# Additional images
- Superficial lymph glands and lymphatic vessels of head and neck.
Degree of polymerization
The degree of polymerization, or DP, is the number of repeat units in an average polymer chain at time t in a polymerization reaction . The length is in monomer units. The degree of polymerization is a measure of molecular weight. For most industrial purposes, lengths in the thousands or tens of thousands are desired.
For a homopolymer, the degree of polymerization may be calculated as shown below
DP = Total MW of the polymer/MW of the repeating unit
In polycondensation, in order to achieve a high degree of polymerization (and hence molecular weight), Xn, a high fractional monomer conversion, p, is required, as per Carothers' equation: Xn = 1/(1p).  A monomer conversion of p = 99% would be required to achieve Xn = 100.

# Correlation with physical properties
Polymers with identical composition but different total molecular weights may exhibit different physical properties.  In general, increasing degree of polymerization correlates with higher melting temperature  and higher mechanical strength.
Dejerine Sottas syndrome
Dejerine-Sottas Syndrome/Neuropathy (hereditary motor and sensory polyneuropathy type III; sometimes also described as a subtype III of Charcot-Marie-Tooth disease) is an autosomal dominant or autosomal recessive neuropathy.

# Symptoms
It is usually characterized by infantile onset of moderate to severe lower and upper extremity weakness and loss of sensation.
Symptoms are usually more severe and rapidly progressive than in the other more common Charcot-Marie-Tooth diseases, and some carriers may never walk and be wheelchair-bound by the end of their first decade, while others may need only a cane (walking stick) or similar support through life.
Symptoms range from very common (muscle weakness, reduced sensation in the extremities, pain in the extremities, clawed hands and deformed feet, ataxia, peripheral areflexia) to rare (hearing loss, nystagmus, anisocoria).

# Diagnosis
On medical imaging, the nerves of the extremities (and cranial nerves in some cases) appear enlarged due to hypertrophy of the connective interstitial tissue, giving the nerves a distinct 'onion-bulb' appearance.   Peripheral (and possibly cranial) nerve excitability and conduction speed are reduced.
Delavirdine microbiology

# Microbiology

## Mechanism of Action
Delavirdine is an NNRTI of HIV-1. Delavirdine binds directly to reverse transcriptase (RT) and blocks RNA-dependent and DNA-dependent DNA polymerase activities. Delavirdine does not compete with template:primer or deoxynucleoside triphosphates. HIV-2 RT and human cellular DNA polymerases , , or  are not inhibited by delavirdine. In addition, HIV-1 group O, a group of highly divergent strains that are uncommon in North America, may not be inhibited by delavirdine.
In vitro anti-HIV-1 activity of delavirdine was assessed by infecting cell lines of lymphoblastic and monocytic origin and peripheral blood lymphocytes with laboratory and clinical isolates of HIV-1. IC50 and IC90 values (50% and 90% inhibitory concentrations) for laboratory isolates (n = 5) ranged from 0.005 to 0.030 M and 0.04 to 0.10 M, respectively. Mean IC50 of clinical isolates (n = 74) was 0.038 M (range: 0.001 to 0.69 M); 73 of 74 clinical isolates had an IC50 0.18 M. The IC90 of 24 of these clinical isolates ranged from 0.05 to 0.10 M. In drug combination studies of delavirdine with zidovudine, didanosine, zalcitabine, lamivudine, interferon-, and protease inhibitors, additive to synergistic antiHIV-1 activity was observed in cell culture. The relationship between the in vitro susceptibility of HIV-1 RT inhibitors and the inhibition of HIV replication in humans has not been established.

## Drug Resistance
Phenotypic analyses of isolates from patients treated with RESCRIPTOR as monotherapy showed a 50- to 500-fold reduced susceptibility in 14 of 15 patients by Week 8 of therapy. Genotypic analysis of HIV-1 isolates from patients receiving RESCRIPTOR plus zidovudine combination therapy (n = 79) showed resistance-conferring mutations in all isolates by Week 24 of therapy. In patients treated with RESCRIPTOR, the mutations in RT occurred predominantly at amino acid positions 103 and less frequently at positions 181 and 236. In a separate study, an average of 86-fold increase in the zidovudine susceptibility of patient isolates (n = 24) was observed after 24 weeks of combination therapy with RESCRIPTOR and zidovudine. The clinical relevance of the phenotypic and the genotypic changes associated with therapy with RESCRIPTOR has not been established.

## Cross-Resistance
RESCRIPTOR may confer cross-resistance to other NNRTIs when used alone or in combination. Mutations at positions 103 and/or 181 have been found in resistant virus during treatment with RESCRIPTOR and other NNRTIs. These mutations have been associated with cross-resistance among NNRTIs in vitro.
Developmental milestones
Developmental milestones are tasks most children learn, or physical developments, that commonly appear in certain age ranges. For example:
- Ability to lift and control the orientation of the head (Neck control) is attained at about 3 months
- Crawling begins at about 7 months
- Walking unsupported is attained at about 12 months
- Speech begins
- Voice lowers in pitch (especially noticeable in boys)
- Pubic hair appears
- Genitals and reproductive organs mature
- Menses begin (females)
- Body hair and facial hair appears
"Normal" age ranges for many milestones are broad (a factor of 1.5 - 2 from bottom to top is possible). For this and other reasons, a single delayed milestone, especially task-related, is rarely in itself a basis for diagnosing a problem.
Note: the Tanner stages can be used to approximately judge a child's age based on physical development.
Dermatographic urticaria

# Overview
Dermatographic urticaria (also known as dermographism, dermatographism or "skin writing") is a skin disorder seen in 4-5% of the population, in which the skin becomes raised and inflamed when stroked or rubbed with a dull object. The symptoms are thought to be caused by mast cells in the surface of the skin releasing histamines without the presence of antigens, due to the presence of a weak membrane surrounding the mast cells. The histamines released cause the skin to swell in the affected areas.
This weak membrane easily and rapidly breaks down under physical pressure causing an allergic-like reaction, generally a red welt to appear on the skin. It can often be confused with an allergic reaction to the object causing a scratch, when in fact it is the act of being scratched that causes a welt to appear. These welts are a subset of hives that appear within minutes, accompanied by a sensation of burning, and/or itchiness. The first outbreak of hives can lead to others on body parts not directly stimulated, scraped or scratched. In a normal case the swelling has reduced itself with no treatment within 15-30 minutes, but in extreme cases, itchy red wheals may last anwhere from a few hours to days.
Dermatographism can be caused by stress, tight or abrasive clothing, watches, glasses, energetic kissing, heat, cold, or anything that causes stress to the skin.  In many cases it is merely a minor annoyance, but in some rare cases symptoms are severe enough to impact a patient's life.
It can be treated by antihistamines or cromoglicate, as they prevent the histamine from causing the reaction. The underlying cause of dermographism is not known, and can last for many years without relief. 95% of chronic cases are never solved. Sometimes the condition goes away, sometimes it stays forever. It is not a life threatening disease.

# Diagnosis

## Physical Examination

### Skin
- Dermatographic urticaria. Adapted from Dermatology Atlas.
- Dermatographic urticaria. Adapted from Dermatology Atlas.
- Dermatographic urticaria. Adapted from Dermatology Atlas.
- Dermatographic urticaria. Adapted from Dermatology Atlas.
- Dermatographic urticaria. Adapted from Dermatology Atlas.
- Dermatographic urticaria. Adapted from Dermatology Atlas.
- Dermatographic urticaria. Adapted from Dermatology Atlas.
- Dermatographic urticaria. Adapted from Dermatology Atlas.
- Dermatographic urticaria. Adapted from Dermatology Atlas.
Desoxymethyltestosterone

# Overview
Desoxymethyltestosterone (Madol) is an anabolic steroid. It was one of the first "designer steroids" to be marketed as a performance-enhancing drug to athletes and bodybuilders. In animal studies it has been found to be a powerful androgen approximately half as potent as dihydrotestosterone, but caused serious side effects that are typical of 17-alkylated steroids, such as liver damage and left ventricular hypertrophy.
Desoxymethyltestosterone is sometimes referred to as "DMT", though it is not the same compound as the hallucinogen Dimethyltryptamine, also known as DMT.
Desoxymethyltestosterone was invented in 1961 by Max Huffman who obtained a patent on the compound. It was never brought to market as commercial drug and existed only in some obscure journal articles until it was rediscovered by chemist Patrick Arnold in 2005. Arnold produced desoxymethyltestosterone and supplied it to Victor Conte of Bay Area Laboratory Co-operative (BALCO), an American nutritional supplement company.
Desoxymethyltestosterone is unusual in that it is structurally a 2-ene compound, lacking the 3-keto group present on nearly all commercial anabolic steroids. This does not mean it is a weak compound, and clinical research has determined that it is a fairly potent oral agent. Rat studies indicate desoxymethyltestosterone has an anabolic effect 160% that of testosterone while being only 60% as androgenic giving it a Q ratio of 6.5:1. Because of this favorable ratio, experiments in orchiectomised rats have demonstrated that treatment with desoxymethyltestosterone resulted only in a stimulation of the weight of the levator ani muscle; the prostate and seminal vesicle weights remained unaffected. In humans, this may mean that it would be less likely to cause unfavorable androgenic side effects like hair loss, acne and prostate enlargement.
Interestingly, although desoxymethyltestosterone is completely synthetic in origin, it is nearly identical in structure to delta2-androstenol, a naturally-occurring pheromone found in elephant urine.
Glycogen storage disease
Synonyms and keywords:Glycogenosis; dextrinosis

# Overview
Glycogen storage diseases are several inborn errors of metabolism that result from enzyme defects that affect the processing of glycogen synthesis or breakdown within muscles, liver, and other cell types. A total of fourteen glycogen storage diseases have been described which differ from each other on the basis of genotypic and phenotypic heterogenity. Most of the glycogen storage diseases follow an autosomal recessive mode of inheritence. In 1929, Von Gierke was the first to describe glycogen storage disease in a 8 year old girl. Glucose-6-phosphatase deficiency found in glycogen storage disease type I is identified as first specific enzymopathy in a hereditary disorder. Majority of glycogen storage diseases are due to deficiency of specific enzymes involved in metabolism of glycogen either in liver or muscle or both. These deficiencies commonly result in excess of glycogen which deposits in several tissues in the body. There are a wide variety of clinical manifestations of glycogen storage diseases. However, common clinical manifestations of various glycogen storage diseases include hypoglycemia, hypotonia, muscle weakness, hepatomegaly, cardiomegaly, elevated creatine kinase, hyperlipidemia, myoglobinuria, and elevated liver aminotransferases.

# Pathophysiology

## Metabolic Pathway

## Gross Pathological Findings
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission.  PEIR, University of Alabama at Birmingham, Department of Pathology
- Pompe's Disease, Glycogen Storage Disease Type II. Child in crib
- Pompe's Disease, Glycogen Storage Disease Type II
- Pompe's Disease, Glycogen Storage Disease Type II
- Pompe's Disease, Glycogen Storage Disease Type II, 9 years old patient
- Pompe's Disease, Glycogen Storage Disease Type II, 9 years old patient
- Pompe's Disease, Glycogen Storage Disease Type II
- Pompe's Disease, Glycogen Storage Disease Type II

## Microscopic Pathological Findings
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission.  PEIR, University of Alabama at Birmingham, Department of Pathology
- Muscle: Glycogen Storage Disease
- Muscle: Glycogen Storage Disease
- Nerve: Glycogen Storage Disease Macrophages; Longitudinal Section of Peripheral Nerve

# Differentiating various Glycogen Storage Diseases

# Heart & Liver in Glycogen Storage Disease
Dicrocoelium dendriticum

# Overview
The Lancet liver fluke (Dicrocoelium dendriticum) is a parasite fluke that tends to live in cattle or other grazing mammals.

# Life cycle
D. dendriticum spends its adult life inside the liver of its host.  After mating, the eggs are excreted in the feces.  The first intermediate host, the terrestrial snail (Cionella lubrica in the United States), eats the feces, and becomes infected by the larval parasites. The larvae (or cercariae) drill through the wall of the gut and settle in its digestive tract, where they develop into a juvenile stage. The snail tries to defend itself by walling the parasites off in cysts, which it then excretes and leaves behind in the grass. The second intermediate host, an ant (Formica fusca in the United States), uses the trail of slime as a source of moisture.  The ant then swallows a cyst loaded with hundreds of juvenile lancet flukes. The parasites enter the gut and then drift through its body, eventually moving to the sub-esophageal ganglion (a cluster of nerve cells underneath the esophagus). There, the flukes, now as metacercariae, take control of the ant's actions by manipulating these nerves. As evening approaches and the air cools, the infested ant is drawn away from other members of the colony and upward to the top of a blade of grass. Once there, it clamps its mandibles onto the top of the blade and stays there until dawn. Afterward, it goes back to its normal activity at the ant colony. If the host ant were to be subjected to the heat of the direct sun, it would die along with the parasite. Night after night, the ant goes back to the top of a blade of grass until a grazing animal comes along and eats the blade, upon which the lancet flukes will be back inside their host. They live out their adult lives inside the animal, reproduce, and the cycle continues.

# Ecological role
The lancet flukes are important to grasslands. To prevent infestation, cattle avoid patches of the greenest grass, which has been fertilized by manure. The danger for them is not the feces themselves, but rather the possibility that tiny ants might be at the tops of the blades, carrying the parasite . Therefore, those patches grow undisturbed as cows feed on the remaining grass, which is not enough for all of them. The cows are then forced to eat the green grass, and for a while the cow population rises. Eventually, the parasites infect the cows. Infected cows eat less and fail to reproduce as frequently. The cow population drops, allowing the grass to regrow. The cow population eventually recovers and returns to being wary of the greenest grass, completing the cycle.

# Treatment

## Antimicrobial Regimen
- 1.Dicrocoelium dendriticum
- Preferred regimen: Praziquantel 25 mg/kg PO tid for 2 days
- Note: Praziquantel is not approved for treatment of children less than 4 years old.
- Alternative regimen (1): Myrrh (commiphora molmol) 12 mg/kg/day PO for 6 days
- Alternative regimen (2): Triclabendazole 10 mg/kg PO single dose