Thingification by Pharma company

Thingification has been honed to a high art by the pharmaceutical
industry, where everyday emotions like sadness, grief, fear, and suffering
are transformed into codified disease. From the industry’s point of
130 What Matters in Medicine
view, the purported chemical imbalance or genetic flaw that underlies
such emotions not only can but should be treated. Where causal proof
or benefit lacks sturdy scientific proof, direct marketing to the consumer
picks up the slack.
There is a way to see the world other than as categories of morbidity
and mortality, digitalized data and discrete behaviors, probabilities and
outcomes. This view relies on emotion and the senses. It seeks context
and connection. It expresses itself through anecdote, vignette, the use of
metaphor, and tales of survival. It is captured—if
at all—in
case reports,
reflective journaling, and the literature of medicine. It blossoms and endures
without having a name, or needing one.

We press ahead with our blinders and prejudices, too busy or proud to ask for directions.

My second patient of the night was an elderly woman who presented
with left-sided
numbness of her face, arms, and legs. Symptoms had
started the day before, and though they had not worsened, they had not
resolved, either. She was particularly concerned that adult-onset
diabetes,
heart disease, and a blood-clotting
disorder (Leiden Factor 5 deficiency)
increased her risk for stroke. She had seen her primary care physician in
his office earlier that day; upon detecting dizziness and upper extremity
weakness, he had sent her to the emergency department for evaluation.
A check of the patient’s vital signs and my neurological exam of her
yielded completely normal results. Her CT head scan was unremarkable.
Had she experienced a TIA? Why did her numbness and tingling
persist? I asked her how she had been sleeping and eating and if she had
been under an unusual amount of stress. After an uneasy silence, she
furrowed her brow and hoisted herself up on her elbows. She explained
that she and her husband have one son, who lives out of state. His job
often takes him away from home, and their daughter-in-
law
has, in effect,
raised their children. Finances are tight, and the patient and her
husband have drawn on their retirement savings to help support their
son’s family. Their daughter-in-
law
had called last week, unbeknownst
to her husband, and insisted on talking to my patient’s husband. He
was told that his grandson had gotten into trouble at school. When the
boy’s father (the patient’s son) had reacted by confiscating his phone, the
boy had threatened to kill him with a knife. Meanwhile, the patient had
heard nothing more from her son or daughter-in-
law.
She could not say
anything to her son, because he did not know that she knew about the
incident. As the patient was talking, I watched as the reading on the self-inflating
blood pressure cuff climbed to 190/110. Her voice was now quivArrival
127
ering, her fingers were trembling, and she nodded meekly when I asked if
the tingling had returned.
In medicine, it is easy to travel far down the road of assumptions
before stopping to ask how or where we have traveled. We do what we
are trained to do; we follow a well-worn
clinical agenda. We press ahead
with our blinders and prejudices, too busy or proud to ask for directions.
Increasingly, we ask computers and assistants to enforce our protocols,
because, frankly, we know they will do a better job. We become distracted,
tired, rushed, and annoyed. We are lured by prior experiences and
competing loyalties. But it takes a generalist physician—in
touch with
one’s instincts and emotional intelligence—to
recognize a clinical dead
end or ill-fitting
puzzle. It takes time—time
that no one has—to
start
over, engage in conversation, reestablish trust, and offer hope that a solution
is still possible.
What should patients expect from their doctor? To have their diagnosis
set aside until someone with the time, training, and desire has
heard every concern, even those you are unwilling or unable to express.
This is the challenge and privilege of primary care. It permeates primary
caregivers’ field of action and rules of engagement:
Patients present with an undifferentiated problem.
The time frame for action is open-ended,
not critical or urgent.
Illness has upset the patient’s routine.
Change is required in order to return to the norm.
Change begins only after the patient accepts personal responsibility;
it is mediated through the patient’s social network.
The doctor-patient
relationship is a starter kit for acceptance and
change.

What Matters in Medicine?

What Matters in Medicine?
Indian Health leaders must realize that

it is in our national interest to maintain a robust primary health care

system. Some see it as a solution to the unsustainable rise in health care

costs, which gathers steam like a runaway train as baby boomers board

for their golden years. Lawmakers, corporate executives, and health care

officials are paying close attention to studies that demonstrate higher

rates of preventive care, improved health outcomes, and lower overall

costs for health care delivery systems that integrate a strong primary care

Component.

I hope to flesh out the work of primary care,

but not from the perspective of an advertising agent, systems analyst,

policy maker, or corporate executive. My view comes from the clinic, and

from living among my patients for most of my professional career. I believe

that the delivery of timely, appropriate, effective, and personalized

care can be achieved, and at a substantial savings in cost. But to do so,

we all need to share in the inherent risks and responsibilities of “getting

better” and to reexamine our biases about health and disease
Decline of the GP

Until World War II, there was only one kind of physician, the generalist,

who was trained as both a general physician and a general surgeon. In

1940, more than three-fourths

of doctors in active practice called themselves

generalists.2 But World War II and its escalating need for tighter

governance and greater specialization altered the landscape of American

medicine.

Specialty boards had, in fact, emerged much earlier—slowly

at first

and then with gathering momentum. Ophthalmology broke the ice in

1916, followed by otolaryngology in 1924, obstetrics and gynecology in

1930, and dermatology and syphilology in 1932. Pediatrics, orthopedic

surgery, urology, radiology, and the combined disciplines of psychiatry

and neurology created specialty boards in 1935, and internal medicine,

pathology, and surgery followed suit in 1937.

During World War II, physicians were organized according to specialty

board, and board-certified

physicians commanded a higher rank

and pay scale. The Veterans Administration paid board-certified-physicians

25 percent more than non-board-certified-physicians,

argued

strenuously for the revival of the generalist physician. This ultimately

led, in 1969, to the approval of family medicine as the twentieth medical

specialty. But it did little to redress the growing imbalance—in

numbers,

prestige, or salary—between

specialists and generalists. By 2008, primary

care physicians (family physicians, general internists, and general pediatricians)

represented only a third of the total workforce actively involved

in patient care.4 The ratio of generalist to specialist physicians in training

fares worse: only a fifth are preparing for practice in primary care.

The causes of the current crisis are multiple and complex. Physicians

in training, under the tutelage of highly specialized clinicians and

surgeons, are given a clear (if implicit) message about the institutional

disregard for general practice. Many rural rotations expose the country

doctor as someone who is overworked and underappreciated. The practice

of primary care requires a temperament and skill set that admission

committees in medical schools typically undervalue: a mastery in

problem solving rather than memorization; an affinity for teamwork .
 It is not enough that researchers, social scientists, and health care
administrators appreciate the value of primary care. Medical schools
and training programs, as social servants of the constituencies that fund
them, are politically and morally obligated to redress the imbalance they
helped create. Patients themselves should act on their enormous stake
in the survival of primary care. They could exercise their considerable
political muscle

Money Makes Many things

There is an obvious mismatch between the needs of the country for
low-cost, high-quality primary care and the career choices of medical
students. A recent survey of medical students found that just 2 percent
were interested in general internal medicine, 4.9 percent in family medicine,
and 11.7 percent in general pediatrics. Between 2002 and 2006, the
percentage of residents in training who intended to enter primary care
practice dropped from 28.1 percent to 23.8 percent. Between 1998 and
2008, 9,100 accredited residency slots were added to the graduate pool in
medical education, but family medicine lost 407 positions (23.3 percent),
and general internal medicine lost 865. Over 40 residency programs in
family medicine and 25 in general internal medicine disappeared in a
single decade.Moreover, the training of greater numbers of midlevel
practitioners has not compensated for the underproduction of primary
care physicians. Only 37 percent of the 80,000 physician assistants are
working in primary care. Half of the 140,000 nurse practitioners are located
in ambulatory settings, but fewer than half of these are directly
involved in primary care.
The 2010 entering class continued the long-standing
trend: 43.4 percent
were from allopathic schools, 18.1 percent from osteopathic schools, and
38.4 percent from the IMG pool.

the cost of administering health care insurance is double the cost of providing primary care to everyone

 With everyone praising the  new insurance schemes  implemented by the south Indian states of  AP/Telangana and Karnataka

Dr. Michael Fine has estimated the cost of population-based primary care to be $500 per person per year in 2003 dollars ($592 in 2010 dollars).10 This includes dental care, primary care laboratory and imaging tests, mental health services, home health care, nutrition counseling,physical therapy, common generic pharmaceuticals, and public health services. By contrast, the cost of health insurance is four to five thousand dollars per person per year, of which 10 to 20 percent, or four hundred to one thousand dollars, is spent on administrative overhead. In other words, the cost of administering health care insurance is double the cost
of providing primary care to everyone.11

I am proud to say I have been working in a Federally qualified health center for the last 5 years.

I am proud to say I have been working in a  Federally qualified health center for the last 5 years.
One of the federal government’s most successful programs is its net-    
work of federally qualified health centers, or community health centers (CHCs). It has been shown that patients who receive the majority of their care at a CHC spend 41 percent (or $1,810) less on medical costs than patients who rely on other providers, representing a savings of be-    
tween $9.9 and $17.6 billion annually. Moreover, health centers pump dollars and jobs into their low-income communities, with an economic  impact that reaches $12.6 billion annually and creates 143,000 jobs. 

 Primary Care
communication instead of individual and technical prowess; humility
and compassion instead of bravado and detachment. Lastly, the financial
ramifications of choosing a career in primary care play a pivotal role. In
September 2010, the Robert Graham Center reported an income gap of
$135,000 between the median annual income of sub specialists and that
of generalists, yielding a lifetime difference of $3.5 million dollars.5 Medical
students, whose average debt at the time of graduation is more than
$140,000,6 recognize the quicker path to solvency.
The late Barbara Starfield and others have shown that certain regions
of the United States and developed countries with a higher ratio of primary
care physicians to specialists are associated with superior health
outcomes. These include lower infant mortality; fewer visits to emergency
departments, hospitalizations, and procedures per capita; and overall
lower health care costs. Patients of primary care providers generally receive
fewer diagnostic tests and procedures. When patients can identify a
usual source of care, especially a regular physician, they are more likely to
receive recommended preventive services, report greater satisfaction with
their care, utilize fewer services, and have lower costs of care. Longer
relationships between Medicare beneficiaries and their usual provider
also reduce hospital admission rates and total cost of care.7 Furthermore,
primary care physicians are much more likely to be located in rural areas,
where you still find 20 percent of the population but less than 10 percent
of practicing physicians. All of this is well known and only grows in
importance as the nation and its primary care workforce age.
.   
 

Indian Innovative Drugs Initiative))2

Examples of possible diseases that IDD( IntrAnasal drug delivery) may be used to treat are Alzheimer's disease, depression, anxiety disorders, seizures, autism spectrum disorders, and drug addiction

polymeric nanoparticle‐facilitated delivery

Lipid nanoparticles

Magnetic nanoparticles.

Cell-penetrating peptides, also called Trojan peptides

A potential non-invasive glioblastoma treatment: Nose-to-brain delivery of farnesylthiosalicylic acid incorporated hybrid nanoparticles

Studies on the non-invasive anticancer remedy of the triple combination of epigallocatechin gallate, pulsed electric field, and ultrasound

several novel drug delivery techniques, including intranasal drug delivery, nanoparticles, drug modifications, convection‐enhanced infusion, and ultrasound‐mediated drug delivery.

There's no placebo effect on a horse

There's no placebo effect on a horse.
How can we tell has anyone  performed any studies?

While talking about  DMSO therapy used by veterinarians. D.Jacob says "There's no placebo effect on a horse."

Indian Innovative Medicines Initiative _DMSO+ glibenclamide tripledrug hairtonic

  Indian Innovative Medicines Initiative

DMSO
Glibenclamide in DMSO IV for large  hemorrhagic CVA  to reduce  brain swelling
Use of topical DMSO/with Diclofenac /Dexamethasone 
MINOXIDIL+Dutasteride+cyproterone  acetate topical for hair growth

Dimethylsulfoxide (DMSO) is a colorless organosulfur solvent, which dissolves both polar and non-polar compounds and is miscible in a wide range of organic solvents as well as in water.

From: Side Effects of Drugs Annual, 2012

Related terms:
Phosphate Chloride Potassium chloride Intravenous therapy Ethylenediaminetetraacetic acidAcetate HEPES Absorption (pharmacokinetics)EthanolAcetone
Learn more about Dimethyl sulfoxide

Laminitis
In Diagnosis and Management of Lameness in the Horse (Second Edition), 2011

Free Radical Scavengers
Dimethyl sulfoxide (DMSO) may be given intravenously for its free radical scavenging and antiinflammatory effects. DMSO (90% solution) mixed with polyionic solutions and 5% dextrose is best administered slowly at about 8 L/h. The concentration of DMSO must remain below 20% to avoid the risk of intravascular hemolysis. However, despite the potential value of DMSO, its promise as an effective laminitis therapy has not been fulfilled. Evidence exists that ischemia, reperfusion injury, and generation of free radicals are not involved in the pathogenesis of horses with laminitis induced with extract of Black walnut.18

Read full chapter

Systemic Inflammatory Response Syndrome
Elizabeth A. Carr, in Robinson's Current Therapy in Equine Medicine (Seventh Edition), 2015

Dimethylsulfoxide
Dimethylsulfoxide (DMSO) has been recommended as a treatment for endotoxemia and SIRS because of its antiinflammatory and reactive oxygen species (ROS)–scavenging benefits. Data on the benefits of DMSO administration in models of equine endotoxemia and reperfusion injury are lacking, but data in laboratory animals suggest that pretreatment with DMSO, before the onset of endotoxemia or ischemia-reperfusion injury, may be beneficial in decreasing cellular injury. The dosage recommendation for DMSO therapy is broad, ranging from 0.1 g/kg to 1 g/kg. DMSO should be diluted and infused as a 10% solution to avoid hemolysis.



Pharmacotherapy of joint and tendon disease
Carl A. Kirker-Head, Hillary Feldmann, in Equine Sports Medicine and Surgery (Second Edition), 2014

Effective dose
Domoso® (Pfizer Animal Health) is commercially available as a 90% DMSO veterinary gel for topical use. Manufacturer recommendations are for liberal application to skin over affected area 2–3 times per day. The total daily dosage is not to exceed 100 grams, and the duration of therapy is not to exceed 30 days. Domoso® (Pfizer Animal Health) is also available as a 90% veterinary solution. The recommended dose for the solution is 0.25–1.0 grams/kg diluted in saline or 5% dextrose solution at a concentration of not more than 10%. The 10% solution is to be given at a slow rate once daily for three days. The solution can be administered orally through a nasogastric tube at a dose of 1.0 grams/kg diluted in 1 liter of water.

Treatment protocosl for equine septic arthritis include the option of joint lavage with lactated Ringer's solution containing 5% to 40% DMSO. Lavage solutions containing DMSO concentrations in excess of 5% have been shown to have detrimental effects upon articular cartilage matrix metabolism. Until further investigation and pharmacokinetic studies can be performed, the concentration of DMSO contained within intra-articular lavage solutions should not exceed 5%.

The manufacturer cautions against the use of non-medical grade DMSO products, which may contain harmful impurities secondary to the distillation process. Washing of the hands and wearing protective rubber gloves before handling DMSO is strongly recommended in order to avoid transcutaneous penetration of potentially harmful substances.



Collection and processing of marrow and blood hematopoietic stem cells
Michele Cottler-Fox, ... John Theus, in Hematopoietic Stem Cell Transplantation in Clinical Practice, 2009

Addition of cryoprotectant
Dimethylsulfoxide (DMSO) is the cryoprotective agent most widely used to cryopreserve hematopoietic stem cells at present. DMSO is a universal solvent capable of stabilizing cell membranes under rapidly changing conditions, preventing intracellular ice crystal formation during freezing and heat release during the period of phase transition. DMSO has been described as toxic to stem cells at room temperature, for which reason investigators have emphasized the need to add it at 4°C to cells prior to controlled-rate freezing and to begin cryopreservation quickly thereafter. A final concentration of 10% DMSO with albumin or human serum is commonly used, with some centers using hydroxyethyl starch to help stabilize cell membranes and reduce the amount of DMSO used to 5%.

A new cryopreservative, Cryostor (BioLife Solutions Inc., Corning, NY), is also available. This compound modulates cellular biochemistry during the freezing process and is free of serum, proteins, and DMSO.



Painful Bladder Syndrome (Interstitial Cystitis)
Philip M. Hanno MD, MPH, in Penn Clinical Manual of Urology, 2007

INTRAVESICAL THERAPY
Dimethylsulfoxide (DMSO) is the only Food and Drug Administration (FDA)-approved medication for intravesical instillation for the treatment of PBS/IC. It is a product of the wood pulp industry and a derivative of lignin. It has exceptional solvent properties and is freely miscible with water, lipids, and organic agents. Pharmacologic properties include membrane penetration, enhanced drug absorption, anti-inflammatory, analgesic, collagen dissolution, muscle relaxant, and mast cell histamine release. Intravesical delivery by urethral catheter of 50 mL of a 50% solution (Rimso-50) allowed to remain in the bladder for 15 minutes and repeated at weekly intervals for 6 weeks is effective in ameliorating symptoms in about 60% of patients for a period of several months to over a year. Some patients who respond to an initial 6-week course are treated monthly for 6 months. Patients emit a garlic-like odor for several hours after treatment and may experience a short-term symptom exacerbation. It is often administered as part of a “cocktail” including 10 mg triamcinolone (Kenalog), 44 mEq sodium bicarbonate, and 40,000 units heparin.

Heparin, an exogenous glycosaminoglycan, can be administered intravesically in sterile water as a single agent. Forty thousand units in 20 mL of sterile water self-administered via catheter by the patients daily and held for 30–60 minutes has been reported beneficial, but no placebo-controlled studies have confirmed efficacy.

In a large multicenter randomized trial, intravesical bacille Calmette-Guérin (BCG) failed to show a statistically significant benefit compared to placebo. Capsaicin and resiniferatoxin, agents that desensitize C fiber afferent neurons, have failed to gain acceptance for intravesical therapy. The possible therapeutic value of intradetrusor injection of botulinum toxin type A is currently being determined in clinical trials. Older intravesical treatments such as chlorpactin, a derivative of bleach originally used to treat bladder tuberculosis, and silver nitrate are rarely used today for treatment of PBS/IC.



Disorders of the Gastrointestinal System
L. Chris Sanchez, in Equine Internal Medicine (Fourth Edition), 2018

Antioxidants
Dimethyl sulfoxide (DMSO) is used by some clinicians in an attempt to scavenge oxygen-derived radicals. However, DMSO failed to show beneficial effects in an experimental model of intestinal ischemia when administered on reperfusion of the ischemic intestine. DMSO at a dosage of 1 g/kg body mass increased mucosal loss after ischemia and reperfusion of the large colon, and a reduced dosage of 0.1 g/kg body mass has been proposed for horses with intestinal ischemia. DMSO failed to show significant benefit in an experimental model of endotoxemia in horses, although it ameliorated the effect on fever, and many clinicians do not advocate its use. The xanthine oxidase inhibitor allopurinol has been suggested as a treatment to prevent oxygen radical–induced tissue damage. During periods of ischemia tissue xanthine dehydrogenase is converted to xanthine oxidase, which on reperfusion catalyzes the generation of superoxide radicals. Evaluation in horses showed beneficial effects of allopurinol 5 mg/kg body mass administered 12 hours before endotoxin challenge. In another study mucosal damage attributable to oxygen-derived free radicals was not attenuated by allopurinol in an experimental ischemia–reperfusion model.



A worldwide yearly survey of new data in adverse drug reactions and interactions
N.H. Choulis, in Side Effects of Drugs Annual, 2012

Dimethylsulfoxide (DMSO) [SED-15, 1131; SEDA-32, 894; SEDA-33, 1015]
Dimethylsulfoxide (DMSO) is a colorless organosulfur solvent, which dissolves both polar and non-polar compounds and is miscible in a wide range of organic solvents as well as in water. It penetrates the skin very readily.

Umbilical cord blood transplantation using non-myeloablative conditioning is currently considered by many as a useful alternative for any patient who requires an unrelated donor allograft and who lacks a suitably matched and readily available volunteer. On the other hand, DMSO has been used for years as a cryoprotectant for umbilical cord blood; it acts by penetrating cells and binding water molecules and it has been described as harmless for the individual who receives it in limited amounts. DMSO-induced adverse reactions have been described in three cases and briefly reviewed; two of the three cases had a poor prognosis [27Ar].

In a review of the published literature, hundreds of adverse reactions, such as nausea, chills, cardiac dysrhythmias, neurological symptoms, and respiratory arrest, have been identified in association with the transplantation of stem cells cryopreserved with DMSO [28M]. These adverse reactions are generally accepted as commonplace, as most of them are transient, although some patients may require treatment.

Skin 

A topical solution of diclofenac sodium in a vehicle containing dimethylsulfoxide has been studied in 793 subjects, mean age 63 years, with radiologically confirmed symptomatic osteoarthritis of the knees, who applied 40 drops qds for up to 1 year [29c]. They used the solution for an average of 204 days; 463 subjects used it for 6 months and 144 for 1 year. The most frequent adverse events were at the application site: dry skin (25%), contact dermatitis without vesicles (13%), or contact dermatitis with vesicles (9.5%); the risks did not increase with prolonged exposure. Skin irritation score was normal in 61% of the subjects: the scores were 0.5 (dryness or flaking) in 24%, 1 or 2 (erythema without or with induration) in 6.9%, and 3 or 4 (erythema with induration and vesicles/bullae) in 8.2%. Dropouts included 114 (14%) with an application site adverse event. There were individual laboratory test shifts towards abnormal for hemoglobin (3.2%), aspartate aminotransferase (6.4%), alanine aminotransferase (7.3%), and creatinine (4.2%), but few of the shifts were clinically significant. There were no increased risks of cardiovascular or cataract events.

Read full chapter

Topical and Transdermal Drug Delivery
S. Narasimha Murthy, H.N. Shivakumar, in Handbook of Non-Invasive Drug Delivery Systems, 2010

1.4.11.2 Sulfoxides and similar solvents
Dimethyl sulfoxide (DMSO) is a powerful aprotic solvent that is colorless, odorless, and hygroscopic. Studies have demonstrated that DMSO is effective in promoting the permeation of a number of hydrophilic and lipophilic permeants. It has been found to enhance the permeation of beta blockers (Kai et al., 1993) and ephedrine hydrochloride (Singh et al., 1993). The enhancer effect is reported to be concentration dependent, with concentrations greater than 60% required to show optimum efficacy (Williams and Barry, 2004). However, erythema and wheals of the stratum corneum have been reported at these relatively high concentrations of DMSO, which have also resulted in protein denaturation (Anigbogu et al., 1995). Human volunteer studies have demonstrated erythema, scaling, contact urticaria, stinging and burning sensations, and some systemic symptoms (Kligman, 1965). The skin penetration mechanisms of the aprotic solvents, and DMSO in particular, are complex. Upon application to human skin, DMSO is known to denature proteins and change the intracellular keratin conformation from helical to β sheet (Oertel, 1997). DMSO is said to interact with the head group of the lipid bilayers to distort the packing geometry. Further partitioning of the drug from the formulation into DMSO present within the tissue is favored.

Another aprotic solvent, dimethylformamide (DMF), is known to enhance absorption through the polar pathway by increasing diffusion and partitioning (Sinha and Kaur, 2000). A 12-fold increase in the flux of caffeine across DMF-treated human skin was observed, though the authors reported irreversible skin damage (Southwell and Barry, 1983). DMF is reported to increase the permeation of ephedrine hydrochloride across rat skin and human epidermis (Singh et al., 1993), and also promote the in vivo bioavailability of betamethasone-17-benzoate (Barry et al., 1984; Bennett et al., 1984).

Other aprotic solvents employed as permeation enhancers include dimethylacetamide, dimethyloctanamide, and dimethyldecanamide. Dimethylacetamide was found to increase the permeation of indomethacin from ointments and creams in rats (El-Faham and Safwat, 1992). Dimethyloctanamide and dimethyldecanamide were found to enhance the permeation of ibuprofen and naproxen from aqueous propylene glycol solutions across rat skin (Irwin et al., 1990). Decylmethylsulfoxide, a structural analog of DMSO, is known to act reversibly on human skin and promote the permeation of hydrophilic permeants (Williams and Barry, 2004). It is reported to increase the flux of oxymorphone hydrochloride through guinea-pig skin and human skin (Aungst et al., 1990a) and 5-fluorouracil across human skin (Goodmann and Barry, 1988).



Dimethyl Sulfoxide Toxicologic Problems
Patricia Talcott, in Equine Internal Medicine (Fourth Edition), 2018

Dimethyl Sulfoxide
Dimethyl sulfoxide (DMSO), a byproduct of the paper-making industry, is a colorless liquid originally used as an industrial solvent. The chemical is a polar compound that readily mixes with ethyl alcohol and many organic solvents; it is extremely hygroscopic and can absorb more than 70% of its weight of water from air. DMSO possesses some antimicrobial and antifungal activity, but its primary medical use has been as an antiinflammatory agent and a transdermal transport agent. More recently, DMSO has been used as a diuretic and has shown promising results when used to treat acute cranial and spinal cord trauma.

The systemic toxicity of DMSO is considered to be low, and its greatest toxic potential appears to result from its combination with other agents. However, in an experimental study rapid infusion of DMSO in 20% and 40% concentrations caused hemolysis, hemoglobinuria, diarrhea, muscle tremors, and signs of colic in some horses. The LD50 of DMSO has not been established for horses, but ranges between 2.5 and 9.0 g/kg as a single intravenous dose have been reported in a number of animal species. A dose of 1 g/kg intravenously has been suggested for use in horses. This dose should be diluted to a 10% to 20% solution and administered slowly intravenously.

DMSO produces hemolysis when given intravenously in concentrations of 20% to 50% or greater. If hemolysis is severe, affected horses may be at increased risk of developing hypoxic nephrosis. Concentrations of 10% or less are considered suitable for intravenous injection in horses. Additionally, increased white blood cell adherence and fibrinogen precipitation have been reported when concentrations greater than 50% were administered.

DMSO is a mild cholinesterase inhibitor, and its concurrent use with organophosphates or other cholinesterase inhibitors is not recommended. DMSO also is known to induce histamine release from mast cells, but the significance of this phenomenon is unclear.

Skin reactions to topically applied DMSO sometimes occur. Varying degrees of erythema, pruritus, drying, hardening, and desquamation of normal skin may be evident. These reactions are usually self-limiting and typically diminish with repeated applications.

The greatest risk of toxicity resulting from DMSO is probably a consequence of its concomitant use with other toxic or potentially toxic agents. DMSO may aid transport of a variety of toxic compounds across skin, thereby inducing toxicosis from the transported agent. For example, mercury toxicity has been reported in a horse that had a blister after DMSO and mercury were applied topically to a leg. In such instances, the clinician should treat the specific toxic reaction (or reactions) appropriately. No specific antidote is recognized for DMSO toxicosis, and it should always be used judiciously and conscientiously. The practitioner should heed the aforementioned precautions when administering the drug.



Globins and Other Nitric Oxide-Reactive Proteins, Part A
Paul R. Gardner, in Methods in Enzymology, 2008

10.1 Reagents
20 mM hemin prepared in dimethyl sulfoxide and stored at −20°

100 mM dithiothreitol in water stored at −20°

Dithionite (solid)

Tris‐Cl (50 mM), pH 8, containing EDTA (1 mM)

Catalase (bovine liver) (2,60,000 units per mL)

To reconstitute heme‐deficient flavohemoglobin with heme, flavohemoglobin is incubated with heme under reducing conditions in the presence of catalase to scavenge potentially damaging peroxide. Briefly, flavohemoglobin (0.5 to 0.75 mM) is prepared in a volume of 1.5 mL containing 50 mM Tris‐Cl, pH 8, 1 mM EDTA, 10 mM DTT, 3000 U of catalase, and hemin is then added slowly from a 20 mM stock in dimethyl sulfoxide to a final concentration of 0.5 mM. Dithionite (≈2 mg freshly dissolved in 25 μL of water) is added after 15 min of incubation to fully reduce hemin and eliminate O2. The reaction is incubated at 37° for 60 min. The flavohemoglobin is then immediately separated from free heme, catalase, and reductants by gel‐filtration chromatography. For this purpose, a 1.5 cm × 60 cm Superdex 200 column equilibrated with N2‐sparged 50 mM Tris‐Cl, pH 8, buffer containing 1 mM EDTA is used.

Medical EDI Electronic Data Interchange

"A paperless hospital office is the goal of the US healthcare system as it provides more efficient, and thus cheaper, data distribution, retrieval, search, and analysis"
The above may be the biggest Hoax of all times 

 What used to be a well thought out,experienced, Medical consultation report  about 1 or 2 paragraphs has become multiple pages of Useless Gibberish. You are forced to search for the grain among the chaff.
I have worked with specialists in various specialities in  1970s and 80s where they would spend  an hour  examining and explaining and interacting with the patient  then  write  2 to 4  absolutely relevant  sentences  or  pickup the phone and  talk to the referring  GP or another specialist.
Now just like  the  useless gibberish of radiology reports consultation reports are useless multi page  gibberish.
In order to understand why this happened is what i am after.
in that process  I need to  find out about the  secret codes ,handshakes,ceremonies of the  new  healthcare informatics.Just like the  masonic codes,handshakes and mysterious  ceremonies.
let us start with a list of  cryptic Acronyms.

 EDI
"To address the problem of rising healthcare costs and to enhance the quality and efficiency of care, the Workgroup for Electronic Data Interchange (WEDI) was formed in 1991 by the Secretary of Health and Human Services (HHS). When the Health Insurance Portability and Accountability Act (HIPAA) was enacted in 1996 establishing national standards for healthcare EDI transactions, the WEDI was one of the instruments used to implement it.

Let’s dig a bit deeper and find out what exactly an EDI is and how it can benefit the entire healthcare system."

Fair Credit Reporting Act (FCRA)

Fair Credit Reporting Act (FCRA) 

What is LOINC, a Universal Standard for Identifying Laboratory Observations:

LOINC, a Universal Standard for Identifying Laboratory Observations:
LOINC, a Universal Standard for Identifying Laboratory Observations:

If you go to  Labcorp or Quest labs  website test Menus  you  see  a bunch of numbers  sometimes in  EHR you find a  bunch of  lab tests in various permutations and  combinations.

They are so many and so confusing most primary care physicians have a few in their Favourites list and use them routinely.

So sometimes more tests are done and sometimes tests which could have been done are missed.

Learn about them so that  we can be  better informed and may help in patient management

 A 5-Year Update
Clement J. McDonald, Stanley M. Huff, Jeffrey G. Suico, Gilbert Hill, Dennis Leavelle, Raymond Aller, Arden Forrey, Kathy Mercer, Georges DeMoor, John Hook, Warren Williams, James Case, Pat Maloney
DOI: 10.1373/49.4.624 Published April 2003
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Abstract
The Logical Observation Identifier Names and Codes (LOINC®) database provides a universal code system for reporting laboratory and other clinical observations. Its purpose is to identify observations in electronic messages such as Health Level Seven (HL7) observation messages, so that when hospitals, health maintenance organizations, pharmaceutical manufacturers, researchers, and public health departments receive such messages from multiple sources, they can automatically file the results in the right slots of their medical records, research, and/or public health systems. For each observation, the database includes a code (of which 25 000 are laboratory test observations), a long formal name, a “short” 30-character name, and synonyms. The database comes with a mapping program called Regenstrief LOINC Mapping Assistant (RELMATM) to assist the mapping of local test codes to LOINC codes and to facilitate browsing of the LOINC results. Both LOINC and RELMA are available at no cost from http://www.regenstrief.org/loinc/. The LOINC medical database carries records for >30 000 different observations. LOINC codes are being used by large reference laboratories and federal agencies, e.g., the CDC and the Department of Veterans Affairs, and are part of the Health Insurance Portability and Accountability Act (HIPAA) attachment proposal. Internationally, they have been adopted in Switzerland, Hong Kong, Australia, and Canada, and by the German national standards organization, the Deutsches Instituts für Normung. Laboratories should include LOINC codes in their outbound HL7 messages so that clinical and research clients can easily integrate these results into their clinical and research repositories. Laboratories should also encourage instrument vendors to deliver LOINC codes in their instrument outputs and demand LOINC codes in HL7 messages they get from reference laboratories to avoid the need to lump so many referral tests under the “send out lab” code.

Today most laboratory and diagnostic systems in the US deliver their results electronically via Health Level Seven (HL7) 1 (1) messages to their hospital, office practice, health maintenance organizations (HMOs), public health departments, and other clients. The HL7 message carries one record for each separate test observation. Within this record is one field that identifies the test, e.g., serum sodium, and another that reports its value, e.g., 142. These observations records carry other fields for reporting the units of measure, the reference interval, normal flag, and other information. In the HL7 nomenclature, the field that carries the observation identifier is called OBX-3, and the field that carries the observation value is called OBX-5. Until recently, most laboratories would send their own local and idiosyncratic codes in OBX-3 to identify the observation. One laboratory would identify serum sodium with the code “C1231” and another with the code “SNA”. Every laboratory had its own unique code for every test observation. This extreme degree of variation is a huge barrier to the development of clinical repositories and research databases for office practices, hospitals, HMOs, and public health departments because mapping these local laboratory codes (thousands of them per laboratory) to the codes used in the receiving systems requires large labor investments. If we had a universal code system for tests and everyone used this system, this barrier probably would vanish, and receiving systems could “understand” and recognize all results that flow to them in HL7 and other electronic messages (2) and efficiently store these results in their medical record or repository system.

Before 1994, no universal pre-coordinated code system for laboratory test names existed, although considerable background work had been done within organizations such as the IFCC/IUPAC Committee/Commission on Properties and Units in Clinical Chemistry (3)(4), and EUCLIDES(5). In 1994, a group of researchers met in Indianapolis at the Regenstrief Institute to begin the development of such a system, which they called the Logical Observation Identifiers Names and Codes (LOINC®) code system. The initial release, in the spring of 1995, included a 70-page Users’ Guide and identifiers and names for more than 6000 laboratory test results (6)(7).

Since this first release, the Regenstrief Institute and the LOINC Committee have delivered 17 releases, increased the size of the database fivefold, added codes for many clinical subjects beyond the laboratory, added short names for laboratory tests, developed and enhanced a free browsing program, the Regenstrief LOINC Mapping Assistant (RELMATM) (8), and watched adoption of the LOINC coding system grow.