Repairing a completely dead Asus ROG G75VW 17-inch Gaming Laptop

December 1st, 2018

This one was fairly uncomplicated:

  • There was a bad 4936N MOSFET near the power jack.  In circuit there was very low resistance between gates, sources, and drains of both MOSFETs. It was not really possible to tell which of the two MOSFETs in that area was bad without removing both the 4936N and the nearby PH5030AL.  After removing both, the 4936N was confirmed bad as it read 15 ohms from gate to drain and 0 ohms from gate to source.
  • Additionally, the Winbond 25Q64FVSIG BIOS chip was visibly fried (cracked package).  You can get a programmed replacement for about USD $20 and I would recommend this unless you are experienced with programming BIOS chips.
  • Using hot air it is easy to remove all of these and install the replacements, but watch the very small capacitor next to the MOSFET and to the left of the JP4601 marking – if you blow it away it’s a headache to get back into place, if you can even find it!  (In this picture it’s next to the 4936N, but on my board the PH5030AL was in that location.)
  • Use a rework flux pen.

You should be good to go for reassembly in half an hour.  To test, just connect the power jack board, the power switch board with the ribbon cable, and a fan, connect power and depress the power switch momentarily and it should spring to life!  Note: If the CPU is not installed and/or the BIOS is inoperative, it is expected behavior that the fan speed will cycle up and down rhythmically.  Once the CPU can execute the correct BIOS code, it will then control the fan speed appropriately.

Reviving a bitrotted OEM Windows Vista installation on your Linux laptop

June 24th, 2018

If you’re a normal sort of Linux user, when you buy a laptop you probably keep that Microsoft OS partition around, shrinking it to a minimal size and allowing it to coexist with Linux just in case you need it for firmware updates, special Windows-only tools for special situations, or sometimes just for an A/B comparison if you suspect something might be wrong with the Linux driver for a particular device.

So, after not booting that Windows Vista partition for a few years, and possibly having gone through a few disk upgrades and associated disk imaging in the meantime, you try to boot it up only to find:

  • It doesn’t boot via the automatically populated GRUB entry, hanging at a black screen
  • It doesn’t boot via Hiren’s Boot CD or another tool booting the Vista partition directly, with a winload.exe “missing or corrupt” BSOD
  • Third-party software upgrades don’t work
  • Windows Update doesn’t work
  • Anything you try to install manually doesn’t work


Well, here’s how you should be able to fix that mess (steps tested on Windows Vista Home Premium OEM 32-bit SP1).

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Can LiteOn/Slimtype DS8A1H laptop DVD recorder burn dual layer DVDs?

April 22nd, 2018

Many mid-2000s Compaq/HP laptops which shipped while DVD media was predominant included this unbranded “Slimtype DVD A DS8A1H” DVD recorder, which is actually a rebadged LiteOn drive.  It’s not that great a drive, but it does work to burn double/dual layer (DL) DVDs for use on a console DVD player.  Here is what you need to know to produce DVDs that work on a console player.

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New directions in dementia reversal

April 15th, 2018

There is no need to restate the impact of dementia on families, institutions, and the social fabric.  Adult-onset dementia is typically diagnosed as Alzheimer’s when one of two conditions is present:

  • Amyloid-beta plaques (amyloidosis; first observed by Alois Alzheimer in 1907 and biochemically profiled by George Glenner in 1984)
  • Hippocampal atrophy in disproportion to global cortical atrophy

The vast majority of research funding to date has been directed at the theory that amyloid-beta plaque and tau tangle formation, consisting respectively of misfolded amyloid-beta and tau proteins, is the root cause of the observable neurodegeneration (neuron death) and symptomatic presentation of dementia.

Two alternative mechanisms to produce misfolded proteins are proposed in this theory: glutamate excitotoxicity, and attacks by reactive oxidative species.  The hypothesis is then that the disease can be stopped by preventing the misfolding from occurring.

I will not address this disease model or hypothesis of treatment as both have been and continue to be thoroughly explored in the literature. However, as no actionable solutions have yet arisen from the depths of this research, and it does not even attempt to address dementias with a non-Alzheimer’s pathology (i.e.: no amyloidosis) I will attempt to redraw the picture on a blank canvas.

(The following is pure conjecture and subject to revision and feedback)

Inflammation and oxidation

Free radicals (molecules which readily oxidize materials with which they come into contact) can be consumed in contaminated or toxic foods, and they can also be produced by the gut flora.  Free radicals are directly toxic to cells through oxidation attacks that produce reactive oxidative species.  Inflammatory cytokines are produced by the actions of free radicals, as well as directly by hostile periodontal and gut bacteria.  Free radicals directly attack the gut lining, while at the same time inflammatory cytokines induce an autoimmune response that misidentifies the gut lining as the source of inflammation and destroys it, causing gut permeability with respect to the blood and to the vagus nerve.

Inflammation and metabolic diseases are linked to Alzheimer’s.  The gut microbiome can contain pathogens which are a source of inflammationFecal transplantation is used in Europe to treat metabolic syndromeIntestinal inflammation is linked to the development of Parkinson’s disease, with the vagus nerve as the suspect vector.  In Parkinson’s, aromatic compounds are excreted in sebum that can be used to identify sufferers with 100% accuracy.

Excess iron is a major contributor to free radical formation.  An elevated body iron level has been linked to heart attack, stroke, cancer, diabetes, and Alzheimer’sCannabidiol was shown to restore memory and mitochondrial function as well as inhibit apoptosis in the brains of iron-overloaded rats.

While the immediate neurodegeneration during a stroke event is likely due to glutamate excitotoxicity, a process which is also involved in epileptic seizures and is entirely deactivated by cannabidiol, it seems that the ongoing neurodegeneration and cognitive impairment subsequent to a stroke is actually caused by central nervous system inflammation, possibly due to dormant bacterial infection.  Perispinal etanercept administration scavenges the inflammatory cytokine TNF from the central nervous system and produces rapid improvement in stroke victims.

While steroids have been used to suppress inflammation in Alzheimer’s victims, scavenging of the TNF cytokine itself by perispinal etanercept administration produces rapid improvement in aged dementia victims, documented on video, for whom chronic inflammation rather than neurodegeneration is presumably the immediate cause of cognitive impairment — although TNF itself has also been shown to produce cognitive impairment even in the absence of neurodegeneration.  One could surmise that this could be because mitochondria switch from producing energy to producing toxins during inflammation.  Cannabidiol has a potent anti-inflammatory (including anti-TNF) and immunosuppressive effect as well.

TNF has been proposed as the culprit in chronic brain dysfunction.  Despite persuasive clinical evidence that eliminating TNF and thus TNF-triggered inflammation restores lost cognitive performance, the theory itself remains unsatisfying because it does not propose a causal mechanism for the production of TNF itself.

Vagal nerve stimulation has been shown to inhibit the production of inflammatory cytokines.

Inflammation from environmental pollution causes Alzheimer precursor anomalies to appear in the brains of infants.

Chronic inflammation is suspected to be the cause of depression and anxiety disorders.

Studies have shown that blueberry powder and blueberry vinegar relieve mild cognitive impairment.  One anecdote further demonstrated that a strict berry, greens, and sweet potato diet initiated a complete recovery of dementia.  Blueberries, as well as blackberries, raspberries, and blackcurrants, contain anthocyanins that have antioxidant effects through mechanisms that are not fully understood.  However, one thing that is known is that blueberries inhibit the production of TNF. Pomegranate extract and juice were independently shown to aid in stroke recovery and to reverse mild cognitive impairment. Individuals in a study who ate approximately one serving of leafy greens per day performed on average as if they were 11 years younger on a standard cognitive assessment test.

Sulforaphane, a phytochemical found in broccoli, cabbages and related vegetables, was claimed in a Chinese study to have triggered neural stem cell proliferation and differentiation into new neurons with no toxicity.

B vitamin supplementation slowed AD-typical brain atrophy in patients diagnosed with mild cognitive impairment.

An anti-inflammatory medical diet fed to mice genetically engineered to develop Alzheimer’s disease completely eliminated the cognitive symptoms while reducing amyloid-beta levels.

Metabolic factors and autophagy

Autophagy impairment is characteristic of Alzheimer’s and other neurodegenerative disorders.  Intermittent fasting has been shown to induce neuronal autophagy.

Insulin resistance is strongly associated with Alzheimer’s and with the underlying amyloid-beta and tau anomaliesInsulin sensitivity (inverse resistance) is increased with high-intensity interval training.  Tying these threads together, as of 2018 regular exercise is officially recommended and drugs considered ineffective in the treatment of cognitive impairment.  A study showed that simply restoring impaired hearing and eyesight significantly slowed the rate of cognitive decline.

Alzheimer’s has recently been unofficially dubbed “type 3 diabetes“.  Alzheimer’s and type 2 diabetes have both been linked to chronic spirochete infection.  Simple carbohydrates such as sugars are the key dietary factors in the insulin resistance model, and it happens that sugars are also the only energy source for most spirochete bacteria.  There is only one spirochete species, Spirochaeta isovalerica which does not use sugars but rather uses the proteinogenic branched-chain amino acids leucineisoleucine, and valine for food.  In this context, it may be of interest to note that athletic supplementation with branched-chain amino acids is suspected to cause an ALS-like syndrome and that individuals diagnosed with ALS have subsequently died of Lyme disease.

Drugs that are commonly prescribed for metabolic issues, such as statins, are known to produce reversible dementia.


Since the early 20th century, periodontal pathogens have been implicated in heart disease, originally due to the observations of dentist Weston Price of heart attacks occurring shortly after root canal work.  Since then, periodontitis has been linked to high blood pressurechronic back pain, and, yes, Alzheimer’s disease.  A C-reactive protein (CRP) test can reveal systemic inflammation rooted in periodontitis.

What’s the connection?  Common periodontal bacteria emit inflammatory cytokines which cause autoimmune destruction of gum and bone tissue and subsequent tooth detachment.  Among those periodontal bacteria are spirochetesOral spirochetes have been shown to migrate through gum tissue into the bodySpirochetes are a key suspect in an infectious model of dementia. Finally, P. gingivalis, the bacterium that causes periodontitis, has been separately implicated in multiple in vitro studies as a cause of Alzheimer’s.


Viruses in the herpes simplex family are implicated in recent research as a root cause of dementia, using mice.  Separately, the HSV1 virus was shown to induce Alzheimer’s-typical plaques and tangles in neural tissue, and the plaques and tangles contained viral DNA; subsequent research showed that untreated herpes simplex (HSV1) and varicella zoster (VZV) infections were associated with a significantly greater risk of later senile dementia.  In the HSV hypothesis, the formation of amyloid-beta plaques is a reactive, protective mechanism, rather than an independent pathological mechanism.  It has been known for decades that herpes simplex viruses are unable to replicate in the presence of the cannabinoid THCThe outcome of utilizing cannabinoids seems to depend on whether inflammation is beneficial or pathogenic in a specific case.

Separately, increased loads of the human herpesviruses HHV-6 and HHV-7 have been confirmed in the brains of deceased Alzheimer’s patientsImmune systems of Alzheimer’s patients showed a decreased response to HHV-6.  For various reasons, active HHV-6 brain infection is very difficult to test for.

Influenza infection was linked to the development of Parkinson’s in birds and mice.  HIV brain infection causes the same biological markers implicated in Alzheimer’s.

A new theory divides Alzheimer’s victims into three categories, and identifies inhalational mycotoxins as the cause of neurodegeneration in the third category.  Patients in this category are typically younger and healthier and may comprise as much as 10% of the patient population.  A treatment protocol is available to halt the neurodegeneration and reverse the cognitive decline.

Lyme disease, which is caused by the spirochete borrelia burgdorferi, commonly causes a variety of cognitive impairments, and causes severe dementia in a small number of cases – including that associated with cerebral infarct (global cortical atrophy), which is reversible by clearing the pathogenSpirochete infection has been characterized as a parasitic symbiotic relationship, in contrast to typical pathogenic bacterial infections.

It should be noted that Lyme disease is notoriously difficult to diagnose because in dormancy it produces false negatives with PCR-based assay, and because many people without active infections carry Lyme antibodies, so the presence of Lyme antibodies in blood serum is also inconclusive.

A new theory of Alzheimer’s pathology is that Lyme and periodontal spirochetes infect the central nervous system and cause the symptoms of Alzheimer’s.  In this theory, these spirochetes are able to hide themselves in neural tissue under a protective biofilm while producing the inflammation and autoimmune response that causes amyloid-beta plaque formation and neurodegeneration.  Lyme biofilms and cystic/granular spirochete configurations were directly observed inside amyloid-beta plaques in 100 out of 100 Alzheimer’s postmortem brain tissue samplesThe presence of microbe biofilms in Alzheimer’s plaques was independently confirmed through staining. Alzheimer’s plaques were found to contain both human-derived and spirochete-derived amyloid-beta proteins. Interestingly, the cannabinoid THC both destroys the amlyoid-beta plaques and inhibits the associated inflammatory response, due to THC’s selective anti-TNF activity. It is worth noting that TNF suppression has been shown to interfere with anti-spirochete antibiotic therapy (another report here); however, that could be a useful property to exploit in identifying a concealed and/or unknown pathogen, as spirochetes are notoriously difficult to culture outside of host tissue. That is, one might conduct an anti-inflammatory protocol with drugs or anti-inflammatory herbs as a ruse to entice the spirochete out of dormancy so that the pathogen could be identified. New testing protocols continue to be developed to meet the diagnostic challenge spirochetes present.

Even when the spirochete is eradicated, inflammation can persist long afterwards. Eradication of spirochetes poses two more problems: animals whose spirochete infections were measurably eradicated were still able to pass active infections to ticks (1, 2, 3), and material from destroyed spirochetes is still able to trigger inflammation. However, levels of inflammatory cytokines are lower in chronically infected individuals (>6 mo.). This may be because the biofilm morphology of spirochetes allows the bacteria to persist in a state that does not activate the host immune system, nor respond to typical long-term antibiotic treatment often utilized against “chronic Lyme”. An antibiotic protocol based on daptomycin has been found to destroy biofilms in vitroTraditional herbal medicine such as cinnamon oil, clove bud oil, oregano/thyme oil, ethyl alcohol tinctures of stevia leaf (and — one might surmise — agents which are capable of dissolving amyloid-beta plaques such as cannabinoids) are demonstrated to be capable of destroying spirochete biofilms in vitro and in tissue samples.  Agents which are known to destroy other microbial biofilms may be of particular service: cinnamon oil was found to destroy Candida and MRSA (1, 2) biofilms, while thyme oil was also found to destroy MRSA biofilmsEpsilon-polylysine, a peptide that is used as a natural food preservative, was found to destroy Pseudomonas aeruginosa and aspergillosis biofilms.  While liposomal encapsulations of oils are typically required to cross the blood-brain barrier, oregano oil has psychoactive effects in its default stateA universal protocol remains elusive; however, Alzheimer’s plaques have been attacked with varying success with the antibiotics clioquinol (2001), doxycycline and rifampin (2003), ceftriaxone (2016), and an antibiotic cocktail (2016).

There is a hypothesis that the root cause of the devastating immune syndrome known as AIDS is actually the spirochete that causes syphilis, and that HIV is merely comorbidThe syphilis spirochete is also capable of causing neurodegeneration and dementia that mimics Alzheimer’s. Treatment with the antibiotic doxycycline reduced the number of Alzheimer’s plaques and relieved cognitive impairment in mice. The Lyme spirochete is present in semen and vaginal secretions, raising implications for non-tick-centric epidemiology.  Intestinal spirochete infection is endemic in homosexual men and HIV-infected individuals.

Celebrity Kris Kristofferson suffered dementia for years and was misdiagnosed with Alzheimer’s before the root cause was found to be Lyme diseaseCommentators rejected the diagnosis of chronic Lyme as facially invalid, but failed to propose an alternative (non-iatrogenic) pathogenesis that fit the same facts. Several cases of reversible dementia rooted in Lyme infection have been documented.

To weave an even more intriguing web, Lyme-infected tick-borne nematode parasites have been found in the brains of multiple sclerosis, brain cancer, and Lewy body dementia victimsDoxycycline, which is also the primary antibiotic used in treating Lyme disease, kills filarial nematodes by killing the symbiotic bacterium generally required in their reproductionA filarial Acanthocheilonema nematode infects around 30% of lone star ticks; however, Acanthocheilonema is one of the few filarial nematodes lacking the symbiont.

Schizophrenia has been linked to endogenous retrovirus infection. Intriguingly, treatment with the antibiotic minocycline was found to reverse schizophrenic symptoms in multiple studies in 2010, 2014, and 2017Minocycline was also found to halt the progression of multiple sclerosis.  Although minocycline is most commonly used as an acne medication, it is in the same tetracycline family as doxycycline, the most commonly used antibiotic in treating Lyme disease.  For some reason, the theorized mechanism of effect of minocycline is primarily anti-inflammatory rather than primarily anti-microbial, even though spirochetes have been stained and cultured from the cerebrospinal fluid of MS patients for nearly a century.  Numerous cases of patients suffering from various mental illnesses and subsequently making a full recovery after an infection with a high fever, or after a bone marrow transplant, have been documented.  Common spirochetes cannot survive above 105.8 degrees Fahrenheit, with optimal reproduction occurring at significantly lower temperatures, and induced hyperthermia/’pyrotherapy’ continues to be utilized in management of persistent spirochete infections.

The Lyme spirochete has been documented to cause new-onset panic disorder (1, 2).  Panic disorder comorbidity with schizophrenia has enough distinct features from other schizophrenia manifestations that it has been suggested this comorbidity should be recharacterizedModerate to severe cognitive impairment is characteristic of schizophrenia, while schizophrenia medications are implicated in brain atrophy.  However, recent research demonstrates that at-risk individuals who later develop full psychosis have a steeper rate of gray matter loss; the authors posit that the missing link between schizophrenia and brain atrophy is neuroinflammation rather than medication.  As it happens, a single 600mg daily dose of the cannabinoid cannabidiol given over 40 months eradicated structural brain differences associated with a high risk of psychosis.

A presentation of stroke which turns out to be rooted in infection with the Lyme spirochete is documented again and again in the literature (1, 2, 3).

(Is there further evidence for spirochete-viral coinfections in various chronic neurological diseases?)

A pathogen ensemble could explain the “mixed pathology” often observed in brain tissue autopsies of dementia patients.

Stem cell neurogenesis

A stem cell treatment has been approved in Japan for Alzheimer’s.  A phase I trial is underway in the U.S. with observed restoration of cognitive performance and hippocampal volume subsequent to injection with neural stem cells derived from waist fat.

However, neuroplasticity and mitochrondrial health may be important factors limiting the success of these treatments.

Whole turmeric contains a terpene ar-turmerone which has been shown in rats to increase the proliferation of neural stem cells as well as their differentiation into healthy neurons.

Neuroplasticity and mitochondria

Neuroplasticity refers to the generation of new synapses, the connections between neurons in the brain’s neural network.  A synapse requires a physical point of contact between two neurons.  A typical synapse occurs at the point where a dendrite of one neuron contacts the dendrite of another neuron.  When neuroplastic conditions are present, new connections are being made through a combination of neurogenesis (increasing neuron density) and dendritic outgrowth.

While neuroplasticity is known to decrease with age, loss of existing dendritic spines is characteristic in Alzheimer’s.  Dendrite loss may be an effect of out-of-control synaptic pruning – an otherwise normal process that is mediated by inflammatory cytokines ‘tagging’ a synapse for destructionLoss of dendrites does not necessarily destroy memories embedded in the neural network, but rather prevents access to them, which can be restored.  It has been found that serotonergic psychedelic drugs, commonly referred to as entheogens, stimulate dendritic outgrowth.  Ketamine, a NMDA receptor antagonist with fast-acting antidepressant qualities, stimulates dendritic spine outgrowth and regrowth of spines damaged by chronic stress in mice.

Entheogens as a family are non-specific serotonin receptor agonists, but primarily bind to 5-HT2 receptors5-HT2 receptor loss is characteristic of Alzheimer’s patients and is implicated in the behavioral and psychological symptoms of dementia.  However, 5-HT2 receptor loss precedes the associated neurodegeneration.  The 5-HT2 receptor loss could be due to downregulation subsequent to serotonin misregulation by a third factor.  One study posits a connection between chronic stress and hyperserotonism which then causes the development of a serotonin resistance. Another study showed that low levels of serotonin transporter protein (SERT) is correlated with dementia, implying that impaired serotonin transport is associated with serotonin receptor loss. If impaired serotonin transport and subsequent serotonin resistance is the mechanism by which 5-HT2 receptor loss follows, a supportive therapy is conceivable in which natural serotonin production is suppressed and simultaneously, a non-monoamine 5-HT2 agonist such as LSD is administered to activate 5-HT2 receptors in its place.

Since the sensory-altering effects of entheogens are caused by their binding to the 5-HT2A serotonin receptor, if psychoactive side effects of entheogen administration are too severe, the side effects can be selectively attenuated with a 5-HT2A blocker.  Curiously, it has been shown that activation of the same 5-HT2A receptor with microdose quantities of a drug similar to LSD potently blocks TNF-alpha induced inflammation in the whole bodyChronic inflammation is suspected to be the root cause of anxiety and depression disordersLSD itself is currently being studied as a treatment for anxiety and depression pursuant to the quantity of anecdotes indicating its efficacy in those diseases.

Where synaptic paths are present, proper synaptic function is dependent on healthy mitochondriaMitochondrial dysfunction is a precursor to Alzheimer’sThe vitamin NR (nicotinamide riboside) has been shown to restore neural mitochrondria function, destroy amyloid plaques, and restore cognitive performance.

Mitochondrial transplants have been effective in reviving degenerated muscle tissue; the healthy mitochondria need not even be injected directly into the degenerated tissue to find their ‘home’.  One could surmise that neural mitochondrial transplant would have a similar safety profile.

Meditation has been shown to increase the proportion of the hippocampus and areas of the frontal cortex relative to other brain regions.  One could surmise that neurons can thus be recruited to different networks according to utilization, important in the context of mental illness.

Mental illness and sleep quality

Moderate to severe anxietydepression, and chronic stress are independent risk factors for dementia.  Pseudodementia is cognitive impairment that is caused by such mental illness rather than an organic process.  Pseudodementia can be treated.  However, it is unclear whether pseudodementia is a separate process from the observable organic processes in dementia.  What we know is that depression and anxiety are comorbid with dementia, with 54% of dementia patients exhibiting both depression and anxiety.  While cause and effect is unclear, untreated anxiety and depression is detrimental to quality of life, whether or not dementia is present or would otherwise follow.  As with various forms of dementia, harmful gut bacteria are increasingly implicated in mental illnesses as varied as anxiety and schizophreniaSchizophrenia could be predicted from the microbiome of patients’ stool samples in one study.

One could surmise that the ineffectiveness of SSRIs in reversing dementia-related depression and anxiety is due to the aforementioned low levels of serotonin transporter protein (SERT) and serotonin receptor loss that are implicated in dementia, and the resulting inference that serotonin itself is critically low or absent such that the SSRI has no effect.

Furthermore, SSRIs are known to disrupt sleep in the elderly, and poor sleep quality is a risk factor for dementia.  The latter study inexplicably excluded REM sleep as an object of study.  A later study found that REM sleep anomalies are indeed a predictor of dementia.  While several mechanisms for the connection of sleep quality to dementia have been explored, the most promising link is an observed increased flow of cerebrospinal fluid (CSF) due to neuron contraction during sleep.

If SSRIs are inappropriate for people experiencing dementia, what else could terminate anxiety and depression?

A variant of cognitive-behavioral therapy called PATH was successful in reducing depression in a population with cognitive impairment and treatment-resistant depression.

Hypnosis has been shown to be effective in reducing cognitive impairment and improving quality of life in dementia patients.

Transcranial magnetic stimulation has been demonstrated to halt Alzheimer’s-related cognitive decline and is currently in a FDA trial.  While TMS is known to alleviate depression and anxiety in non-Alzheimer’s patients, whether that effect maps to Alzheimer’s patients with their differing serotonin configuration is unknown.

The dissociative anesthetic ketamine has recently been shown to be the most powerful and fastest-acting antidepressant yet known, confirming widespread anecdotes of its efficacy against treatment-resistant depression and relatively minor side effects.  In mice, an immediate antidepressant effect is followed by dendritic spine outgrowth accompanying persisting antidepressant effects.  Interestingly, ketamine is also a NMDA calcium channel blocker; under the glutamate excitotoxicity theory of dementia, it therefore serves the same purpose as the widely prescribed Alzheimer’s drug, memantine, in blocking the calcium ion channel that – the theory holds – excessive levels of glutamate would otherwise overactivate.  However, cannabidiol prevents glutamate excitotoxicity with a much better safety profile and fewer side effects than agents acting on NMDA receptors.

The serotonergic psychedelics psilocybin, LSD, and MDMA have all been shown to alleviate treatment-resistent depression and/or PTSD.  Since they bind directly to serotonin receptors, they can be effective even in individuals with low and/or misregulated serotonin.

Nicotine has been shown to control depression, and its use is widely observed in mentally ill populations as a suspected form of self-medicationNicotine use has been shown to be preventive of Alzheimer’s and Parkinson’s and improves cognitive performance, with studies still ongoing in the areaNicotine is also a known anti-inflammatory and immunosuppressant.  One could surmise that since an autoimmune process triggered by chronic inflammation is implicated in various forms of dementia, nicotine’s benefits are in that it is suppressive of the autoimmune reaction as well as the underlying inflammatory cytokines.

Delivery problems

While several agents like curcumin, resveratrol, cannabidiol, and the steroid etanercept are known to have, variously, effective amyloid-beta destruction and inflammatory cytokine scavenging effects as well as anti-oxidant effects, delivering those agents to the central nervous system poses a challenge because of intestinal absorption, conversion in the liver, and the blood-brain barrier (BBB).  While active systemic inflammation increases the permeability of the blood-brain barrier, and an agent can be engineered to cross a healthy blood-brain barrier, an ingested agent still has to be either properly absorbed by the gut or leak through the gut lining to enter the blood in the first place.

The “Longvida” formulation of curcumin is an example of a liposomal encapsulation.  It is able to deliver curcumin, a powerful antioxidant, anti-inflammatory, amyloid-beta plaque inhibitor, and autophagic stimulator, to the central nervous system via the BBB.  Liposomal encapsulation is also used with resveratrol, a polyphenol found in red wine.  When delivered to the central nervous system across the BBB, liposomal resveratrol is a potent antioxidant and amyloid-beta scavenger.

The vagus nerve is an important nerve that connects the brain stem to the heart, lungs, and gut in order to exercise control of involuntary body functions such as bowel motility.  Constipation is extremely common in older individuals and dementia patients, and one could surmise that neurodegeneration of the vagus nerve or the brain stem is the root cause.  The carotid sheath is a conduit for the vagus nerve.  Topical application of essential oils to the ganglia of the vagus nerve behind the ears is anecdotally effective in delivery of those oils to the nerve.  Since the vagus nerve connection to the gut is also implicated in the development of Parkinson’s disease, with direct observation of Parkinson’s proteins being transported from the gut to the brain, one could reason that beneficial agents could traverse the vagus nerve as well, perhaps via the carotid sheath as a conduit.  A study showed via fluorescent analysis that the cells of the intestinal lining are connected directly to vagal neurons via synapse-like structuresLaser stimulation of the gut lining stimulated the release of brain dopamine in mice, further illustrating a direct gut-brain connection.

As discussed above, etanercept is a steroid, immunosuppressant, and potent TNF scavenger.  Perispinal administration of etanercept is performed via injection into the external vertebral venous plexus, after which it diffuses through the cerebrospinal venous system.  Historically, cocaine was administered in a similar manner.  Perispinal administration can be roughly considered a lower-risk and less complicated form of an epidural injection.

Aromatherapy has seen a variety of applications, with mostly anecdotal results and not much in the way of peer-reviewed, double-blind studies.  However, a plausible mechanism for the delivery of aromatherapy agents to the central nervous system comes in the unlikely form of the brain-eating amoeba, a freshwater pathogen that enters the central nervous system via the nasal olfactory nervous passageways.  One could reason that a vaporized aromatherapy agent could enter the central nervous system in the same manner.

Google Pixel Phones With Android Oreo Repeatedly Disconnect From Wi-Fi

February 28th, 2018

There is a long thread in the Google support forums which links to several other long threads regarding Google Pixel phones with Android Oreo 8.0 or 8.1 repeatedly disconnecting from WiFi access points that work for other users.  There are multiple causes, some of which were fixed in the January security patch, so here’s the TL;DR.  (As you can see, factory resetting should be a last resort rather than a first resort in this case.)

  • Delete Verizon “Security & Privacy” app, or at least turn off WiFi security, on branded phones.
  • Disable all Chromecast devices on the network to prevent a flood condition when the phone first comes online.  This problem was fixed in the January security patch.
  • Disable 5GHz on a dual-band wireless access point.
  • Set a static IP for the phone in the router DHCP configuration.
  • Use WPA to secure your wireless access point instead of the obsolete WEP standard.
  • Turn on Bluetooth.
  • Disable IPv6 in the router configuration.
  • Reboot in ‘safe mode’, then disable and re-enable WiFi and see if it stays connected.  If it does, reboot normally and then:
    • Force-stop the Google Home app, disable and re-enable WiFi.
    • Force-stop the Waze app, disable and re-enable WiFi. (This was the fix for my phone on Oreo 8.1, as improbable as it may be.)


1990 Honda Accord radiator fan is not running, overheating in traffic

July 16th, 2017

This summer has been a hot one and I noticed that my 1990 Honda Accord began to overheat while crawling along in traffic. A quick triage revealed that the radiator fan was no longer running at all. In the end, the fix was to bypass a broken wire in the main wiring harness. More details below.
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Install Linux on an Android-Based Lenovo Yoga Book (YB1X90F)

April 28th, 2017

Having a Linux distribution installed on an Android netbook can be the best of both worlds. Leveraging the Linux kernel already running on any Android device, a Linux userspace will be native and fast and come with many tools power users will appreciate. Here are some ways to get the most out of the Linux on Android experience.

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APC AP9584 USB Conversion Kit and APC Serial Smart-UPS

April 26th, 2017

The AP9584 serial-to-USB conversion kit for older APC UPS models with a serial host interface is the manufacturer-endorsed solution for interfacing such older UPS units with a USB-based host computer. However, it is specified on the label for “use with APC Back-UPS and Back-UPS Pro only”. Will it work with a Smart-UPS unit?

Initially, it would seem so – all the variables are read properly. However, after a period of 30 days or so, and generally unnoticed to the operator, the “LB” (Low Battery”) status flag is flipped on, while nothing is actually wrong with the battery. This does not cause an immediate problem. However, the next time the UPS does a periodic self-test, the “OB” (“On Battery”) status flag will be temporarily set as is expected during a self-test cycle. However, from the perspective of UPS monitoring software, the combination of LB and OB means “The UPS is nearly dead, so shut down the system cleanly”. As a result, every system listening to the UPS monitoring software would immediately (and cleanly) shut down, and then dutifully wait for a UPS power-cycle that never came!

  • I thought at first this was an anomaly with the particular UPS (Smart-UPS 1500), so I switched to a Smart-UPS 1000. Same result.
  • I thought then that I had just gotten a defective cable, and bought another AP9584 to test. Same result.
  • I then replaced the AP9584 with a good old APC 940-0024C and a Kawamall USB to DB9 (male) serial converter. After months, the problem never happened again!

The Kawamall USB to serial converter has USB vendor:device 1a86:7523 corresponding to a QinHeng Electronics HL-340. Others have noted that Prolific converters also seem to work.

In any case, don’t bother trying to use the APC AP9584 on a Smart-UPS – there seems to be a bug that will cause your systems to be powered off unexpectedly. Just use a normal USB-to-serial converter with the APC 940-0024C or similar smart monitoring cable.

ACPI Warning: SystemIO range X conflicts with OpRegion Y error

April 23rd, 2017

On a Linux system, you might be trying to use a utility like decode-dimms to read the SPD EEPROM of your system’s RAM DIMM modules.

But it does not work, and checking the kernel messages, you see:

[    1.457863] i801_smbus 0000:00:1f.3: enabling device (0001 -> 0003)
[    1.457945] ACPI Warning: SystemIO range 0x0000000000000400-0x000000000000041F conflicts with OpRegion 0x0000000000000400-0x000000000000040F (\SMRG) (20160831/utaddress-247)
[    1.458063] ACPI: If an ACPI driver is available for this device, you should use it instead of the native driver

In this case, the Intel 82801 SMBus driver is attempting to load, finding that the ACPI SMRG (System Management Region) has already claimed part or all of the SMBus I/O range, and failing due to strict ACPI resource enforcement. (In the general case, this will be true of whatever driver is attempting enablement immediately preceding the ACPI messages.)

To work around this and accept the risk of system instability, add the acpi_enforce_resources=lax parameter to your kernel command line and reboot.

Afterwards you will see two extra lines in the output:

[    1.457863] i801_smbus 0000:00:1f.3: enabling device (0001 -> 0003)
[    1.457945] ACPI Warning: SystemIO range 0x0000000000000400-0x000000000000041F conflicts with OpRegion 0x0000000000000400-0x000000000000040F (\SMRG) (20160831/utaddress-247)
[    1.458031] ACPI: This conflict may cause random problems and system instability
[    1.458063] ACPI: If an ACPI driver is available for this device, you should use it instead of the native driver
[    1.458110] i801_smbus 0000:00:1f.3: SMBus using PCI interrupt

The third line is new and appears advisory, but it is actually advising that the device is being enabled despite the risk of instability posed by two kernel drivers owning the same I/O region. The fifth line is from the driver that was attempting to load and its appearance means that it has proceeded to load.

While this parameter might bypass SMBus conflicts in particular, allowing a utility like decode-dimms to offer functionality not offered by the ACPI BIOS that first claimed that I/O region, it will also bypass this conflict for any device affected by ownership by the ACPI BIOS that would prevent a driver from loading.

How to use fio to stress test a hard drive

April 23rd, 2017

So you’ve a got a disk in your hand that’s new, used, or questionably refurbished, and you want to give it a thorough thrashing to see how it holds up before trusting your data to it. How? SMART tests and badblocks are the usual tools, but you really want to simulate a workload instead of just doing a linear once-over.

Fortunately, the fio benchmarking tool has a randrw module that can do exactly this. Run this and it will scribble all over a disk and check the results. You should then have a good idea whether that disk is a winner or a dud for a real world workload.

Example, assuming we will stress-test the disk for 1 day (86400 seconds), we have 4 CPU threads, and the disk to be tested is /dev/sdg (WARNING: all data on this disk will be randomly trashed):

# fio --name=randrw --time_based --runtime=86400 --ioengine=libaio --iodepth=64 --rw=randrw --bs=4k --direct=1 --numjobs=4 --filename=/dev/sdg