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Seismic Noise Has Dropped by up to 50%, allowing quieter earthquakes to be detected. That’s me you hear yelling.

2020-04-09
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a photo of me, by me, looking quizzical. I’m not mad, really I’m not. Or we’re all mad here.

This morning I posted a link to a NYT story that had multiple bits of new information.  One of the more important bits (that I didn’t get to this morning) was that seismometers all over the world have responded to the lockdown orders that have some 90% of the world’s population staying home other than for essential activities.  I personally was little affected by that order (even though I live in California).

As a result of that “stay at home” order, we (not I) are mostly staying at home.  I still take walks in the splendid isolation of my abode among the peach and almond trees.  I still go to the pharmacy for the medications that I take, most important of which is ibuprofen.  I still go to the grocery store.  All my banking needs are taken care of online and most of my bills are paid online.

My wife is still working as a physician assistant.  We still fill up the gas tank on our Toyota Highlander.  Nothing has changed except that I am posting to this blog more frequently.

Yet the seismometers say the world is quieter, and as a result we can hear the smaller earthquakes and the little things that are just the earth’s crust moving around.  What is more, the air quality in Los Angeles has greatly improved.  Now wouldn’t it be grand if all of the people who were running around like chickens with their heads cut off would just stay still?

I know, that’s terribly cynical.  I do feel bad, very bad, for all the people who are dying miserably, alone, because they are under quarantine or isolation in the hospital.  Yet human existence is suffering, or so the Buddha says.

So, if you meet the Buddha on the road, kill him.  Or don’t.  I’d rather you didn’t.  You don’t have to follow every ridiculous instruction you get, do you?

Only follow an instruction if it makes sense– or if you can make sense out of it, which means you may have to think about it for a while.

What did the Buddha mean when he said, if you meet the Buddha on the road, kill him?  Let me know if you figure out what it means.  I’ll be sitting here, quietly listening.

Patients with mild COVID-19 still produce antibodies to SARS-COV-2: MedRxiv, Institut Pasteur, France

2020-05-27

Coronavirus by Engin Akyurt via pixabay.com (open access)

A study from the Institut Pasteur in Paris was published on the preprint server MedRxiv on May 19 (full text .pdf file here).  In this study, healthcare workers were recruited to assess antibodies to SARS-COV-2 (the spike protein) after they had recovered from mild COVID-19 confirmed by RT-PCR tests (nasopharyngeal swabs).  None of the patients required hospitalization during their illnesses.  Their median age was 32, and most were medical students, doctors, or nurses.  Of the 160 participants, 74 had known contact with virus patients at work and 38 met virus-infected people away from a “health care setting”.  The rest apparently had unknown contacts and may have been infected by asymptomatic carriers.

One hundred and fifty five (96.9%) had symptoms consistent with COVID-19 (dry cough, fever, dyspnea, anosmia or ageusia). The median time between onset of symptoms and PCR testing was 2 days (IQR:1-4), and the median time from onset of symptoms to blood sampling was 24 days (IQR: 21-28, range 13-39).

159 of the 160 participants had detectable antibodies to SARS-COV-2 spike protein, with higher levels noted later after the illness (the earliest sample was taken 13 days after onset.) The only participant who had no detectable antibodies was a 58 y/o man who had persistent symptoms 18 days after onset of illness, when blood was drawn for the test.  91% of the participants also had neutralizing antibodies to the virus, with a maximum of 97% after 28 days.  In the discussion, the authors relate that other studies showed higher antibody titers with more severe disease; in this study, virtually all patients with mild disease developed antibodies.

This study demonstrates that patients who recover from mild COVID-19 will develop antibodies, most of them demonstrating neutralizing ability against the virus.  In animal studies, neutralizing antibodies have shown immunity against re-infection; thus, even mild disease should confer protection.  Additional findings:

Interestingly, in our study, individuals with factors associated with more severe disease (e.g., male sex, high body mass index and high blood pressure), were more likely to have high titers of neutralizing antibodies compared to others. This may be due to a higher antigenic burden in such individuals, which will generate a stronger humoral response, or may, on the contrary, suggest that some antibodies may play a deleterious role during infection [15]. Future studies are warranted to characterize the beneficial or detrimental role of specific antibodies in COVID-19 patients and the minimal titer required for protection.

This study was publicized in a story in the Guardian on May 27.  The story states that the study was prompted by multiple illnesses reported after an evangelical retreat in Mulhouse, France in early March– what they described as a “super-spreader” event.  The study was said to be focused on the 80% of people infected who develop mild disease.  Earlier studies were conducted on patients after hospitalization for severe illness.  “Early reports had suggested an absence or limited presence of antibodies in some individuals with mild symptoms.”

This contributes to our understanding that COVID-19 illness results in immunity for the vast majority of those affected, even with mild disease.  Previous reports had questioned the development of antibodies in patients who were not severely ill.  Based on prior experience with SARS-COV-1, immunity is expected to last at least two years.

What happened in 1918, when an influenza pandemic killed 50-100 million people worldwide? We know a lot now, including the genetic identity of the virus–but not everything..

2020-05-26

asthma cigarettes by M Maggs courtesy of pixabay.com

In the spring of 1918, a new form of influenza (H1N1) swept over the world, abating in the summer only to return worse than ever in the fall, not ending until the early summer of 1919.  Three waves swept over the world, in spring 1918, fall 1918, and January 1919.  A third of the world’s population is thought to have been affected and virtually every country suffered to some degree.

Unlike previous forms of influenza, young adults seemed to be the worst affected.  Theories that a cytokine storm caused adult fatalities have not been fully confirmed.  According to Wikipedia, ” Instead, malnourishment, overcrowded medical camps and hospitals, and poor hygiene, all exacerbated by the recent war, promoted bacterial superinfection“– and pneumococcal pneumonia killed many people after prolonged immobilization in bed.

All of the countries involved in prosecuting the World War imposed censorship on their newspapers, leading to little discussion of the pandemic.  Neutral Spain, however, did not censor news reports, leading some to think that the illness was coming from Spain– thus the popular name, “Spanish flu.”  From a Vox article on the 1918 pandemic from March 20, 2020: “John M. Barry : The government lied. They lied about everything. We were at war and they lied because they didn’t want to upend the war effort. You had public health leaders telling people this was just the ordinary flu by another name. They simply didn’t tell the people the truth about what was happening.”

Despite numerous theories as to its origin, no conclusive evidence for any particular epicenter has come to light.  Some evidence points to an origin long before 1918, possibly as early as 1915.  Recent studies of reconstructed virus suggest that its last common ancestor appeared between 1913 and 1916.

Regardless of origin, there is some evidence that the H1N1 strain started in birds (possibly chickens) or pigs and jumped to humans.  English troop stationing camps in Etaples, France and Aldershot, UK both experienced outbreaks of flu-like illness with high mortality rates.  Etaples, in particular, treated soldiers affected by gas attacks, which damaged the lungs.  American troops at Fort Riley in Kansas experienced an outbreak in March 1918, which is often said to be the point of origin.

Massive troop movements spread the virus from England and the United States to France in 1918.  Increased travel within the US also played a role, as men were called up and war bond drives attracted crowds.  There is not enough information to estimate deaths in many countries, but it is clear that the “Central Powers” (Germany, Austria-Hungary, the Ottoman Empire, and Bulgaria) suffered greater infection and death rates even than the Allies.  The pandemic stalled the German spring offensive of 1918– and may have caused the loss of the war.

The virus that caused the 1918 pandemic has been recovered from frozen bodies of Eskimo (Inuit) victims and others and reassembled.  Infection of monkeys with the virus caused deaths from “cytokine storms” so that may explain much of the mortality observed in young adults.  However, malnutrition and overcrowding must also have played a role.  Another cause of widespread infection was neglect of what we now call “social distancing”, both in the military in troop camps and among civilians.  A parade in support of the war bond drive in Philadelphia led to a sudden spike of infections and deaths there in October 1918.

There are many lessons that can be learned from careful study of the 1918 pandemic.  We should have been able to control the spread of COVID-19 within the US based on what we already know about pandemics.  Physical or “social” distancing is critical in reducing rates of infection before a vaccine is available.  Treatments can prevent or relieve the “cytokine storm”.  Transfusion of plasma from recovered patients was found helpful then and is now being done again.  For additional information, refer to the Wikipedia articles on the “Spanish” flu and research on the original, reconstructed virus.

 

 

South African hospital outbreak: at least 119 infected from one emergency room patient; 15 of 39 hospital patients died: Science magazine

2020-05-26

Durban, South Africa by Liesl Muhl courtesy of pixabay.com

Krisp.org published a story on May 22 (which is excerpted in Science magazine on May 25) about an outbreak in a Durban, South Africa hospital that started on March 9 with a patient who entered the emergency room with symptoms of COVID-19.  The infection jumped to another patient who was in the ED (emergency department) at the same time and was admitted to C-ICU (cardiac intensive care unit) with symptoms of a stroke.  From there, the virus spread, apparently mainly through “indirect contact and fomite transmission” to patients on at least five wards.  119 cases at the hospital (80 staff and 39 patients) were affected, and “smaller outbreaks” occurred at a nursing home (four cases) and an outpatient dialysis unit (nine patients and eight staff).  A total of up to 135 cases may have been seeded from one patient attending the emergency room.

Eighteen genomes were sequenced, and all had the same clade: type A2, associated with infections from Europe.  There was “limited genomic diversity” in these genomes, suggesting that all of them came originally from one infection.

Fifteen of the 39 patients infected died, all with multiple co-morbidities and all “elderly.”  “There was no evidence” that “any specific intervention” would have prevented their deaths once they were infected (none of the patients received remdesivir.)  The first opportunity for prevention of additional infections was when an 81 y/o woman (patient 3) (who turned out to have a “transient ischemic attack” (TIA), a precursor to stroke) developed an unexplained fever on March 13.  This woman was discharged from the medical ward to the nursing home on March 16 and readmitted with severe pneumonia on March 22.  During her time on the medical ward, she appears to have infected five other patients on the same ward, although she had no cough or other apparent symptoms except for the transient fever.

Around the same time, a 46 y/o woman (patient 4) (one of the five mentioned above) was admitted with an “acute respiratory illness” on March 21.  Two other patients and a nurse were infected by this patient.  On March 23, a nurse from the C-ICU (who had treated the TIA patient) was found to have confirmed COVID-19.

Patients 3 and 4 appear to have infected nine other patients when they were in the medical intensive care unit between March 22-27.  Patient 7, one of those nine, then infected eight other people on medical ward one.

Patient 8, from medical ward one, was moved to surgical ward one, where he infected two other patients and then died on April 1.  Patient 12 was moved from medical intensive care on March 31 (when it was closed because of the infection cluster) to the surgical intensive care unit, where he infected eight other patients.

A total of 1892 patients were recalled because they had been in the hospital in March; 191 were brought in for testing, and seven of these tested positive.  Some of these patients may have been infected outside the hospital, but it is also possible that some of the 1700+ patients who were not called in for testing had asymptomatic COVID-19 and were missed (that detail is not mentioned in the complete report.)

The case fatality rate among the confirmed COVID-19 cases who were patients (rather than staff) was 38.5%, with a median age at death of 79.  All of those who died had some co-morbidity, eleven with hypertension (high blood pressure), seven with diabetes mellitus (DM), and two with cancer.  None was known to be HIV positive.  In all but three cases, patients who died were not intubated because of their known poor prognosis at the time the decision was made.

A total of 1171 staff members were tested at least once, of whom 80 (roughly 5%) had positive tests.  The positive staff members were mostly from the medical intensive care unit and medical ward one; none of them came from the specialized COVID-19 intensive care unit, possibly due to the extra care taken there against infections.  All staff members eventually recovered; only fourteen were admitted to the specialized COVID-19 ward.

The nursing home involved took care of patient 3, and four other patients there developed COVID-19.  These were isolated in a separate building and no staff members at the home tested positive.  Nineteen COVID-19 cases (11 patients and eight staff) were found at the dialysis unit.  All patients and staff at the dialysis unit (133 and 36, respectively) were tested.  Five of the eleven cases in dialysis (45.5%) died.

A failure of personal protective equipment and infection control procedures (IPC) led to the spread of the virus to a total of 135 people, with fifteen deaths.  It should be noted that there were only two known patients in South Africa with COVID-19 at the time the first patient was seen.

The article recommends separation of patients at low and high risk for COVID-19, with separate entrances.  They recommend environmental cleaning to reduce fomite transmission, “aligned with national COVID-19 IPC guidelines and the national IPC framework manual”, plus monitoring of cleaning with fluorescent markers and visual re-inspection.

In addition,  they recommend physical distancing within the hospital with floor markings and signs.  Finally, they recommend weekly PCR (polymerase chain reaction) (from sputum or nasopharyngeal swabs?) testing of all frontline staff.

The only difficult ask in this country would be weekly testing of frontline hospital staff, but the recent increased availability of test kits should be beneficial here.  Additionally, the throat/sputum test recently developed should make testing much easier and quicker to implement– with no need for staff involvement in specimen collection and a much less invasive procedure than the nasopharyngeal swab that has been the exclusive method so far.

This tragic series of events should be studied by infection control professionals in all hospitals and the lessons learned should be implemented universally if a recurrence with multiple fatalities is to be prevented.

A .pdf file of the comprehensive report is available here and makes for very interesting reading.  It has details of how each infected person interacted with the previous person, thus how the virus was passed on from person to person.

The article states, “KRISP has been created by the coordinated effort of the University of KwaZulu-Natal (UKZN), the Technology Innovation Agency (TIA) and the South African Medical Research Countil [sic] (SAMRC).”  One of the authors is the director of the Nelson R Mandela School of Medicine at UKZN in Durban, South Africa.

Multisystem inflammatory syndrome in children (MISC), a rare and underdiagnosed complication of COVID-19: LA Times

2020-05-25

Madagascar periwinkle–photo by PixArc courtesy of pixabay.com

The Los Angeles Times has an article in its May 22 science section about the Multisystem Inflammatory Syndrome in Children (MIS-C) that has been appearing since the pandemic started.  This condition is very rare but has killed at least three children recently.  It resembles Kawasaki disease (fever, rash, and swelling of hands and feet)– which occurs in about 5,500 children in the US every year– and occurs some three weeks after infection.  Kawasaki disease usually affects younger children, mostly under 5, but MIS-C can occur as old as adolescence.

The symptoms of MIS-C also include red eyes and tongue, abdominal pain, low blood pressure, and diarrhea.  In some cases, it resembles toxic shock syndrome (a condition that occurs when infection causes a reaction with low blood pressure, rash, and prostration) that happens rarely after a tampon is infected with toxin-generating bacteria.

Since the syndrome appears so long after SARS-COV-2 infection, most patients will test negative on the nasopharyngeal swab that detects the antigen.  Instead, an antibody test on the blood is required.  Four patients in Los Angeles had antibody-proven COVID-19 and later developed MIS-C.

Treatment of MIS-C is supportive, similar to treating Kawasaki disease.  First, intravenous immunoglobulin is given, just as plasma from recovered COVID-19 patients has been tried in adults.  Repeat doses of immunoglobulin are often needed.  Aspirin, steroids, and cytokine blockers are added.  Anticoagulants and platelet blockers are needed for the blood-clotting complications.

Three of the four patients treated at Children’s Hospital of Los Angeles have recovered.  The fourth is improving and out of the intensive care unit.  The condition was actually first noticed in the United Kingdom (UK) about a month after the pandemic started; it has not been described in China.  The second place it was found was in New York City, where the pandemic was raging last month.  Three children there have died.

The cause of Kawasaki Disease is unknown; some believe that it is due to some environmental element, such as an infection.  MIS-C is clearly related to the pandemic of COVID-19, but there is suspicion that a genetic element is at work making some children more susceptible.  Further study of the few cases that have appeared is ongoing.

Buddhism versus the Dokkodo of Miyamoto Musashi

2020-05-25

Be Here Now– photo by Harald Lepisk courtesy of pixabay.com

The Dokkodo (The Way I go alone) of Miyamoto Musashi has many parallels to the Buddhist rules.  To take the most important example for me, the first of his  Nine Rules is “Do not think dishonestly.”  This is similar to “Don’t lie”, which is high on the Buddhist lists.  It doesn’t say, though, not to lie to other people, but what is more important to me, don’t lie to yourself.  Or, as another philosopher has said, first be true to yourself, then you can’t be untrue to anyone else.

There are also rules against sexual misconduct, although the Dokkodo has it in more personal terms.  There, he says, don’t have sexual thoughts, don’t crave things that are pleasurable.

I don’t see any rules in Musashi against killing people; that’s to be understood in relation to the Bushido (samurai code) of killing lots of people, especially your opponents in battle and commoners who annoy you.  Consistent with the killing philosophy, the Dokkodo says “Weapons are of the highest importance.”

Buddhists are clear that you’re not supposed to kill or harm anyone.  We see, however, many people who are nominally Buddhist attacking others in society who oppose them– so there is some hypocrisy there.

There is no rule in Musashi against stealing, but there are rules about not wanting things that you don’t need.  You don’t need to steal if you don’t want anything.

The Dokkodo says, in a distinct difference from Buddhism, “I will honor Buddha and the gods, but I will expect nothing from them.”

Even more important to me, Miyamoto Mushashi’s nine rules say: “Pay attention even to trifles” but “Do nothing which is of no use.”

Thus I’m ending this post now, to avoid doing something which is not really useful: talking too much.

A tale of two drugs: Hydroxychloroquine (HCQ) and Remdesivir. Remdesivir lowers death rates, but HCQ is associated with higher death rates.

2020-05-25

photo by Petra Goeschel courtesy of pixabay.com

Hydroxychloroquine (HCQ) has been relentlessly touted by a certain political figure, who even claimed to be taking the drug himself.  He also claims that there is support from doctors and that some studies show it is good.  This is unfortunately not true.  A VA study with 368 patients published on April 21 found an elevated death rate in the HCQ group as opposed to no drug or combined HCQ (HC) and azithromycin (AZ): “Rates of death in the HC, HC+AZ, and no HC groups were 27.8%, 22.1%, 11.4%, respectively.”  A large multicenter study published in Lancet on May 22  had similar results:

96 032 patients (mean age 53·8 years, 46·3% women) with COVID-19 were hospitalised during the study period and met the inclusion criteria. Of these, 14 888 patients were in the treatment groups (1868 received chloroquine, 3783 received chloroquine with a macrolide, 3016 received hydroxychloroquine, and 6221 received hydroxychloroquine with a macrolide) and 81 144 patients were in the control group. 10 698 (11·1%) patients died in hospital. After controlling for multiple confounding factors (age, sex, race or ethnicity, body-mass index, underlying cardiovascular disease and its risk factors, diabetes, underlying lung disease, smoking, immunosuppressed condition, and baseline disease severity), when compared with mortality in the control group (9·3%), hydroxychloroquine (18·0%; hazard ratio 1·335, 95% CI 1·223–1·457), hydroxychloroquine with a macrolide (23·8%; 1·447, 1·368–1·531), chloroquine (16·4%; 1·365, 1·218–1·531), and chloroquine with a macrolide (22·2%; 1·368, 1·273–1·469) were each independently associated with an increased risk of in-hospital mortality. Compared with the control group (0·3%), hydroxychloroquine (6·1%; 2·369, 1·935–2·900), hydroxychloroquine with a macrolide (8·1%; 5·106, 4·106–5·983), chloroquine (4·3%; 3·561, 2·760–4·596), and chloroquine with a macrolide (6·5%; 4·011, 3·344–4·812) were independently associated with an increased risk of de-novo ventricular arrhythmia during hospitalisation.
These findings are discouraging for proponents of HCQ.  The results for remdesivir are much better.  Gilead’s scientists released their most recent study details in the New England Journal of Medicine (NEJM) on May 22:
Preliminary results from the 1059 patients (538 assigned to remdesivir and 521 to placebo) with data available after randomization indicated that those who received remdesivir had a median recovery time of 11 days (95% confidence interval [CI], 9 to 12), as compared with 15 days (95% CI, 13 to 19) in those who received placebo (rate ratio for recovery, 1.32; 95% CI, 1.12 to 1.55; P<0.001). The Kaplan-Meier estimates of mortality by 14 days were 7.1% with remdesivir and 11.9% with placebo (hazard ratio for death, 0.70; 95% CI, 0.47 to 1.04). Serious adverse events were reported for 114 of the 541 patients in the remdesivir group who underwent randomization (21.1%) and 141 of the 522 patients in the placebo group who underwent randomization (27.0%).
It is important to note that the study was prematurely terminated because the time to recovery was significantly shorter for remdesivir, although the difference in mortality did not reach statistical significance.  The death rate was strikingly less with remdesivir: 7.1% versus 11.9% for placebo, a hazard ratio of 0.70– even though that result did not reach statistical significance because the study was stopped early.
There is strong data for the efficacy of remdesivir and the toxicity of HCQ based on these studies.  The mechanisms of action for these two drugs supports these conclusions.  With remdesivir, the drug is incorporated into the growing RNA chain as it is built and terminates it, (Wikipedia) damaging the virus’s genetic code.  HCQ only increases the pH of the vesicle (bag) (Wikipedia) that the virus creates when it fuses with the cell membrane; although this might help, it is not dispositive.  The side effects of HCQ overwhelm this mechanism and result in a higher death rate.
Remdesivir probably works better when it is given very early in the course of COVID-19, when there is active and uncontrolled virus replication.  It is less likely to help during the late phase of severe illness, when “cytokine storm” causes inflammatory reactions all over the body.  This hypothesis has not been confirmed by experiment, but is highly reasonable given experience with other viral infections.  For example, treating the shingles (varicella, or chickenpox) virus effectively requires starting acyclovir or valacyclovir early on (Mayo clinic webpage for shingles.)

Eighteen Bodhisattva Precepts

2020-05-22

Gandhara Buddha circa 1900 years ago, courtesy of wikimedia commons

More lists, this time precepts (from Wikipedia); most importantly, do not teach emptiness to those whose minds are unprepared.  Confusing; that might mean me, because I don’t think my mind is fully prepared.

Eighteen things NOT to do, still ascribed by Tibetan Buddhists and sworn to by monks:

  1. Praising oneself or belittling others due to attachment to receiving material offerings, praise and respect.
  2. Not giving material aid or (due to miserliness) not teaching the Dharma to those who are suffering and without a protector.
  3. Not listening to others’ apologies or striking others.
  4. Abandoning the Mahayana by saying that Mahayana texts are not the words of Buddha or teaching what appears to be the Dharma but is not.
  5. Taking things belonging to the BuddhaDharma or Sangha.
  6. Abandoning the holy Dharma by saying that texts which teach the three vehicles are not the Buddha’s word.
  7. With anger depriving ordained ones of their robes, beating and imprisoning them or causing them to lose their ordination even if they have impure morality, for example, by saying that being ordained is useless.
  8. Committing any of the five extremely negative actions: (1) killing one’s mother, (2) killing one’s father, (3) killing an arhat, (4) intentionally drawing blood from a Buddha or (5) causing schism in the Sangha community by supporting and spreading sectarian views.
  9. Holding distorted views (which are contrary to the teaching of Buddha, such as denying the existence of the Three Jewels or the law of cause and effect etc.)
  10. Destroying towns, villages, cities or large areas by means such as fire, bombs, pollution or black magic.
  11. Teaching emptiness to those whose minds are unprepared.
  12. Causing those who have entered the Mahayana to turn away from working for the full enlightenment of Buddhahood and encouraging them to work merely for their own liberation from suffering.
  13. Causing others to abandon their Prātimokṣa vows.
  14. Belittling the Śrāvakayāna or Pratyekabuddhayāna (by holding and causing others to hold the view that these vehicles do not abandon attachment and other delusions).
  15. Falsely stating that oneself has realised profound emptiness and that if others meditate as one has, they will realize emptiness and become as great and as highly realized as oneself.
  16. Taking gifts from others who were encouraged to give you things originally intended as offerings to the Three Jewels. Not giving things to the Three Jewels that others have given you to give to them, or accepting property stolen from the Three Jewels.
  17. Causing those engaged in calm-abiding meditation to give it up by giving their belongings to those who are merely reciting texts or making bad disciplinary rules which cause a spiritual community not to be harmonious.
  18. Abandoning either of the two types of bodhicitta (aspiring and engaging).

Here are the Sixteen Soto Zen Precepts, some of which are basic to all Buddhism:

The Three Treasures

  • Taking refuge in the Buddha
  • Taking refuge in the Dharma
  • Taking refuge in the Sangha

The Three Treasures are universally known in Buddhism as the Three Refuges or Three Jewels.

The Three Pure Precepts

  • Do not create Evil
  • Practice Good
  • Actualize Good For Others

These are also known as the Three Root Precepts, and are mentioned in the Brahma Net Sutra as well.

The Ten Grave Precepts

  1. Respect life – Do not kill
  2. Be giving – Do not steal
  3. Honor the body – Do not misuse sexuality
  4. Manifest truth – Do not lie
  5. Proceed clearly – Do not cloud the mind
  6. See the perfection – Do not speak of others’ errors and faults
  7. Realize self and others as one – Do not elevate the self and blame others
  8. Give generously – Do not be withholding
  9. Actualize harmony – Do not be angry
  10. Experience the intimacy of things – Do not defile the Three Treasures

The first four of the ten grave precepts are straightforward and are mentioned in all the lists of prohibitions.  The next six are less clear.  “Do not cloud the mind”– does this mean not taking intoxicating substances?  The others show significant similarities to the previous lists I have posted.  All of this is highly preliminary and requires a lot more thought (on my part– it may be clear to you…)