Covid male sterility papers + HPV, herpes

as previously discussed:

https://onlinelibrary.wiley.com/doi/10.1111/andr.12859

A recent report published in JAMA Network Open revealed that in an analysis 38 semen samples from COVID-19 patients, 6 (four at the acute stage of infection and, alarmingly, two who were recovering) tested positive for the virus by RT-PCR.1 Importantly, at this point, we have no idea whether the actual virus was viable and infectious. Nevertheless, the possibility that this coronavirus could have a pathophysiological impact on the testes was suggested by additional data indicating that active COVID-19 infection dramatically reduced the testosterone-to-LH ratio, suggesting a significant impact on the responsiveness of Leydig cells to LH stimulation.2 In many ways, we should not be surprised by these observations because the blood-testes barrier is known to offer little defense against viral invasion, given the wide range of pathogenic viruses (HIV, hepatitis, mumps, papilloma) that are known to be capable of damaging the testes and rendering the host infertile.

Furthermore, the spike protein that gives the COVID-19 virus its corona is known to target ACE2 (angiotensin-converting enzyme 2), which is highly expressed by several cell types in the testes including Leydig cells, Sertoli cells, and the germ line. As a result of these factors, several opinion pieces have been published already, raising the possibility of testicular damage and infertility consequent to COVID-19 infection.24 

However, it is also possible that the virus could gain access to male germ cells once they leave the testes, either in the epididymis or following ejaculation. In this Opinion Article, I shall be focusing on this post-testicular route of infection pointing out, for the first time, that the mature spermatozoon has all of the machinery needed to bind this virus, fuse with it, and even achieve reverse transcription of the viral RNA into proviral DNA. Such considerations raise the possibility that spermatozoa could act as potential vectors of this highly infectious disease. This happens in insects5—why not us?

IN ADDITION TO-

https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.26667

The other side of COVID-19 pandemic: Effects on male fertility

RECONCILE ABOVE WITH

The outbreak of novel coronavirus disease 2019 (COVID-19) has become a major pandemic threat worldwide. According to the existing clinical data, this virus not only causes respiratory diseases and affects the lungs but also induces histopathological or functional changes in various organs like the testis and also the male genital tract. The renin-angiotensin system (RAS), also ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2.

Because the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases. As the COVID-19 pandemic has affected the male genital system in direct or indirect ways and showed a negative impact on male reproduction, this paper focuses on the possible mechanisms underlying the damage caused by COVID-19 to the testis and also other components of the male genital tract.

SO THE SPIKE PROTEIN ALONE TARGETS ACE2, FOUND IN THE BALLS, LIKE URINE* (*THAT PART WAS A JOKE)

and they wanna force all young men to get it

college age men too

and all young women

when other papers cite it might act like an STD?

Huh.

Highlight:

  • The male genital system presents high ACE 2 expression therefore, it will be highly important to investigate and clarify the relationship between COVID-19 and the male genital tract.

I’m not even a man but I can feel my lady balls shrink reading that.

If we look at the mechanisms of these changes caused by SARS-CoV-2 in the testis, as mentioned above, this virus uses ACE 2 for entry into the cells through its surface spike (S) proteins. S proteins have two subunits, S1 and S2, which are responsible for receptor recognition and membrane fusion. Studies have shown that SARS-CoV-2 enters into the host cell through the binding of its C-terminal domain of the S1 subunit to ACE 2. Additionally, some studies have reported that the level of autophagy receptor SQSTM1/p62 in SARS-CoV-2 infected cells has increased, suggesting a decrease in autophagy flux.

So, SARS-CoV-2 itself or via ACE 2 can directly induce or inhibit the autophagy pathway to achieve virus survival.

As a result, SARS-CoV-2 may cause male reproductive disorders by regulating the level of autophagy in male germ cells.4 On the contrary, another hypothesis is that testis degeneration in the COVID-19 cases is attributed to an increase in testicular temperature as an indirect effect of the inflammation.5

or :-

Do the jabs cause inflammation?

Can spike proteins microwave your balls? Do they nuke your little swimmers?

BUT WAIT. THERE’S MORE.

Another molecule effective at entering the cell of the SARS-CoV-2 is host proteases like transmembrane serine protease 2 (TMPRSS2), which cleaves the viral S protein to induce a conformational change that allows to a fusion of the virus and host cell membranes.34 TMPRSS2 is the key molecule for the successful infection process.35 

This protease is more expressed in human tissues than ACE 2; co-expression of ACE 2 and TMPRSS2 has been shown in the testis, endometrium, and placenta. Researchers investigated the coexpression of these two molecules in the testis and accordingly, they found that ACE 2 is predominantly expressed in myoid cells, spermatogonia, Leydig, and Sertoli cells, while TMPRSS2 is expressed in spermatogonia and (elongated) spermatids of the testicular tissue34 (Figure 3).

I warned you about endometriosis-like function. Maybe naturally having endo is protection?

It’s lifelong inflammation. Kinda like cancer. You literally have to cut the tissues out.

Like Fight Club, they’d have to take your balls.

Shocked men aren’t more protective of their bollocks and demanding ONE safety study.

ModRNA has owners. Repossession is plausible, legally.

STD angle:

“Recent studies have reported that SARS-CoV-2 is easily found in human bodily fluids.35 The presence of a virus in a semen sample is still a topic of discussion and research due to the small number of studies. For example, two different studies have analyzed SARS-CoV-2 presence in semen samples and according to these studies, SARS-CoV-2 (+) semen samples were found in two patients from 23 cured patients and four patients from 15 patients in the acute phase. Another study reported that SARS-CoV-2 was not detected in the semen samples of 34 COVID-19 patients.31

“It is also known that the prostate gland secretes prostate fluid, one of the main seminal components, and muscles of the gland help in pushing the seminal fluid through the urethra during ejaculation.31 The critical point is that, as we mentioned above, a small percentage of the prostate hillock and club cells express ACE 220 and also TMPRSS2 is highly expressed by the epithelium of the human prostate;37 so it is more likely to get SARS-CoV-2 infection, which may affect its secretions.31 

These mechanisms could explain  the SARS-CoV-2 (+) semen samples of the studies.23

“If the presence of the virus in semen is definitively proved by studies, assisted reproduction techniques will also be affected. For instance, testing all male patients like HIV or Hepatitis B/C cases, and using appropriate sperm washing techniques, or paying extra attention to sperm freezing for COVID-19 positive patients.35

“Like SARS-CoV-2, most viruses enter the human body through nasal and oral routes, and viral particles may break the blood-brain barrier.” but don’t worry about shedding?

“It has been reported that the brain cells (glial cells and neurons) also express ACE 2 receptors, making them a possible target to induce neuronal death for SARS-CoV-2. Importantly, the central nervous system plays a critical role in endocrine control and spermatogenesis.31 

The Hypothalamic-Pituitary-Gonadal Axis (HPGa) exerts a vital role in reproduction; in other words, HPGa can inhibit the body’s reproductive functions via hormones.3138

We have our mechanism for sterility, people.

Gonadotropin-releasing hormone (GnRH) expressing neurons from the hypothalamus secretes GnRH and it activates the release of the follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland. A low level of GnRH causes a decrease in FSH and LH, resulting in impaired function of the Sertoli and Leydig cells.31 Ma et al.39 showed that COVID-19 patients had significantly higher serum LH levels but decreased testosterone/LH and FSH levels than healthy men, suggesting potential hypogonadism. Taken together, patients with COVID-19 have been found to present a reduced testosterone/LH ratio, indicating possible subclinical damage to male gonadal function.5 Additionally, activation of the HPGa and subsequent alterations in hormone concentrations play a critical role in poor sperm quality.38

Therefore, besides its direct effects on testis, SARS-CoV-2 may affect fertility indirectly via the central nervous system.31

Like a remote control, for your balls.

In conclusion, all preliminary findings mentioned above suggest that the COVID-19 pandemic affects the male genital system in direct or indirect ways and shows a negative impact on male reproductive health, inducing spermatogenic failure. Additional studies are necessary to answer all the questions and further investigations are warranted, but ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2. As the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases.

SPERMATOGENIC FAILURE

and onward

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13654

Could COVID-19 have an impact on male fertility?

duh

The pandemic caused by Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to several hypotheses of functional alteration of different organs. The direct influence of this virus on the male urogenital organs is still to be evaluated. However some hypotheses can already be made, especially in the andrological field, for the biological similarity of the SARS-CoV and SARS-CoV2. As well as SARS-CoV, SARS CoV-2 uses the ‘Angiotensin Converting Enzyme-2’ (ACE2) as a receptor to enter human cells. It was found that ACE2, Angiotensin (1-7) and its MAS receptors are present, over in the lung, also in the testicles, in particular in Leydig and Sertoli cells. A first hypothesis is that the virus could enter the testicle and lead to alterations in testicular functionality. A second hypothesis is that the binding of the virus to the ACE2 receptor, could cause an excess of ACE2 and give rise to a typical inflammatory response. The inflammatory cells could interfere with the function of Leydig and Sertoli cells. Both hypotheses should be evaluated and confirmed, in order to possibly monitor fertility in patients COVID-19+.

Specific genes relating to male fertility have already been found e.g.

https://onlinelibrary.wiley.com/doi/full/10.1002/mrd.23314

oddly recommended with covid papers?

Male infertility is a rising problem around the world. Often the cause of male infertility is unclear, and this hampers diagnosis and treatment. Spermatogenesis is a complex process under sophisticated regulation by many testis-specific genes. Here, we report the testis-specific gene 1700102P08Rik is conserved in both the human and mouse and highly expressed in spermatocytes. To investigate the role of 1700102P08Rik in male fertility, knockout mice were generated by CRISPR-Cas9. 1700102P08Rik knockout male mice were infertile with smaller testis and epididymis, but female knockout mice retained normal fertility. Spermatogenesis in the 1700102P08Rik knockout male mouse was arrested at the spermatocyte stage, and no sperm were found in the epididymis. The deletion of 1700102P08Rik causes apoptosis in the testis but did not affect the serum concentration of testosterone, luteinizing hormone, and follicle-stimulating hormone or the synapsis and recombination of homologous chromosomes. We also found that 1700102P08Rik is downregulated in spermatocyte arrest in men.

Together, these results indicate that the 1700102P08Rik gene is essential for spermatogenesis and its dysfunction leads to male infertility.

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13712

As the incidence and severity of SARS-CoV-2 are reported to be higher in males than females, Shastri et al. performed a study to determine the time to viral clearance after infection in a total of 68 individuals (48 males and 20 females) with median age of 37 years (Shastri et al., 2020).

They observed that females were able to achieve viral clearance significantly earlier than males.

Furthermore, a serial follow-up evaluation of three families with both male and female patients demonstrated that female members of the same household cleared the SARS-CoV-2 infection earlier in each family (Shastri et al., 2020). In order to determine the reason for delayed clearance in males, they also checked the expression of ACE2 in tissue-specific repositories.

It was found that testicular tissues were one of the tissues showing ACE2 expression in 3 independent RNA expression databases (Human Protein Atlas, FAMTOM5 and GETx). Interestingly, the ovarian tissue showed very low expression of ACE2 (Shastri et al., 2020).

so women may be the red herring here

ACE2 and fat study, so expect fatty side effects

https://onlinelibrary.wiley.com/doi/full/10.1111/dth.13989

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13791

Impact of COVID-19 and other viruses on reproductive health

They admit the male HPV link I posted about previously.

Male infertility is linked to some viral infections including human papillomavirus (HPV), herpes simplex viruses (HSV) and human immunodeficiency viruses (HIVs). Almost nothing is known about severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) effect on fertility. The possible risk factors of coronavirus disease 2019 (COVID-19) infection on fertility comes from the abundance of angiotensin-Converting Enzyme-2 (ACE2), receptor entry of the virus, on testes, a reduction in important sex hormone ratios and COVID-19-associated fever. Recent studies have shown a gender difference for COVID-19 rates and comorbidity. In this review, we will discuss the potential effect of COVID-19 on male fertility and talk about what needs to be done by the scientific community to tackle our limited understanding of the disease. On the other side, we will focus on what is known so far about the risk of COVID-19 on pregnancy, neonatal health and the vertical transfer of the virus between mothers and their neonates. Finally, because reproduction is a human right and infertility is considered a health disease, we will discuss how assisted reproductive clinics can cope with the pandemic and what guidelines they should follow to minimise the risk of viral transmission.

Remember, viral entry via SPs cause inflammation that might cause sterility? WELL-

Virus entry begins when the virus surface enzyme called Spike (S) glycoprotein binds to the angiotensin-converting enzyme 2 (ACE2) located on the host cell membrane (Hoffmann et al., 2020; Wang et al., 2020). S protein contains two different domain regions: S1 and S2, each one has its own role in virus entry. S1 domain is the part that binds directly to the host ACE2 receptor while the S2 domain helps the virus to fuse with the target cell membrane using its functional elements (Glowacka et al., 2011; Hoffmann et al., 2020). This process is also mediated by a Transmembrane Serine Protease 2 (TMPRSS2) located on the surface of the target cell membrane used for the priming of the S protein causing the virus entry (Hoffmann et al., 2020; Shen, Mao, Wu, Tanaka, & Zhang, 2017; Wang et al., 2020).

When the fusion of the virus with the target cell membrane occurs, the virus releases its genome and using the host cell organelles to replicates its RNA and releases new mature virion to target other cells (Boopathi, Poma, & Kolandaivel, 2020; Jiang, Hillyer, & Du, 2020) Figure 1.

wait wait wait the wild virus replicates its RNA too?

minor flex –

3.1 Human papillomavirus (HPV) and its impact on male fertility

Human papillomavirus (HPV) is a non-enveloped DNA virus and sexually transmitted worldwide. In some cases, it causes either warts or precancerous lesions (Ljubojevic & Skerlev, 2014). More than 170 HPV types have been identified and completely sequenced (Chouhy, Bolatti, Pérez, & Giri, 2013). Recent studies suggest that HPV infection affects male fertility. In cases of idiopathic asthenozoospermia, HPV DNA was observed in the sperm cells of infertile patients (Foresta et al., 2010; Lee, Huang, King, & Chan, 2002) confirming its role of infertility. Strong association between HPV infection and impairment of sperm parameters, especially a reduction in sperm motility and concentration, was observed in HPV-infected men (Garolla et al., 2012; Jeršovienė, Gudlevičienė, Rimienė, & Butkauskas, 2019). Garolla and coworkers (Garolla et al., 2012) reported that HPV can bind to the head of a spermatozoon and impair sperm motility in men. Certain sperm DNA exons undergo apoptotic fragmentation on HPV-infected men suggesting that HPV types degrade different exons of important genes (Lee et al., 2002). Collectively, these evidences suggest that HPV plays a role in male factor infertility.

3.2 Herpes simplex viruses (HSVs) and their impact on male fertility

Herpes simplex viruses (HSVs) are enveloped DNA viruses of the family Herpesviridae. HSVs include two distinct viruses HSV-1 and HSV-2 (Whitley & Roizman, 2017). HSVs are sexually transmitted and targets reproductive system. HSV-1 causes oral and, occasionally, genital sores while HSV-2 is common cause of genital herpes which may lead to infertility problems in both males and females. HSV DNA was detected in semen from about 50% asymptomatic infertile males (Amirjannati et al., 2014; Bezold et al., 2007; Monavari et al., 2013; Neofytou, Sourvinos, Asmarianaki, Spandidos, & Makrigiannakis, 2009). A strong association of HSV infection and low sperm count, poor motility, and increased apoptotic cells were reported (Monavari et al., 2013). Haematospermia and a lower seminal volume and abnormal viscosity were found in HSV-2-infected males which indicate prostate dysfunction (Kurscheidt et al., 2018). Bezold et al. (2007) reported significantly reduced sperm concentration and motility as well as reduced citrate concentrations and neutral α-glucosidase in HSV-infected males, suggested impaired epididymal and prostate function.

The manwhore diseases are listed alongside HIV, lol.
The wages of sin is death, in men as well as women.
How will PUAs recover? They won’t. God Willing.

The concern show that SARS-CoV-2 may affect male reproductive organ and thus results in male infertility stems from several observations. Early studies both in China and Italy showed that males are more susceptible to COVID-19 compared to females (Guan et al., 2020; Livingston & Bucher, 2020).

A recent large cohort observational study from United Kingdom featuring around 20 thousands COVID-19 patients reported that males represented 60% of cases and considered the male sex as one of the risk factors for COVID-19 (Docherty et al., 2020).

DS: MRAs: crickets

More alarming is the result of a new systematic review—included 48 recently published articles and 16 databases—where it found that men are more likely to suffer or to die from the complications of COVID-19 compared to women (Serge, Vandromme, & Charlotte, 2020).

DS: suffer or die? Binary?

Large proportion of these vulnerable males is in their childbearing age, and thus their reproductive ability can be affected.

Finally, like influenza, COVID-19 patients suffer from fever, which may affect sperm production. It was reported that febrile illnesses had an impact on semen parameters (Sergerie, Mieusset, Croute, Daudin, & Bujan, 2007). Total sperm count and motility percentage were reduced significantly at days 15, 37 after fever episode before going back to normal after several weeks (Sergerie et al., 2007). Increase of sperm DNA fragmentation index and alteration in the nuclear protein composition of ejaculated spermatozoon were reported after fever episode (Evenson, Jost, Corzett, & Balhorn, 2000).

Different viruses use different routes to enter into the host cells. SARS-CoV-2 uses the same ACE2 receptor used by its cousin, the SARS-CoV virus, with the help of TMPRSS2 (see Figure 1). Single cell expression analysis has detected the expression of ACE2 RNA not only in the lung epithelial cells, but also in several other organs, among them are the kidneys and the bladder (Fan et al., 2020; Lin et al., 2020; Tipnis et al., 2000). Protein expression analysis also confirmed the presence of ACE2 protein in multiple tissues (Hamming et al., 2004).

Interestingly, the highest expression of ACE2 was found in the testes (Fan et al., 2020). The high expression of the ACE2 receptor in the testes raises a concern that the SARS-CoV-2 has the route to enter some if not all testicular cells and thus could cause damage.

To further analyse the types of testicular cells vulnerable for SARS-CoV viruses, Wang et al. studied single-celled ACE2 expression in the human testes (Wang & Xu, 2020). They found that ACE2 is mainly expressed in spermatogonia, leyding and Sertoli cell, while spermatocytes and spermatids had very low expression (Wang & Xu, 2020). Interestingly, TMPRSS2 expression is similar to ACE2, where TMPRSS2 was also enriched in spermatogonia and spermatids. It has been also shown that ACE2 positive spermatogonia cells express genes that are important for virus reproduction and transmission, while ACE2 positive leyding and Sertoli cells express genes that are required for cell–cell junctions and immunity.

Collectively, these results highlight the risk of COVID-19 on testicular cells and on the spermatogenesis process.

The only direct evidence for the effect of COVID-19 on male reproductive function comes from a study where sex hormones namely testosterone (T), luteinising hormone (LH) and follicle-stimulating hormone (FSH) among others were compared between COVID-19 patients and healthy controls. While the T level was not different between the two groups, the ratio of T to LH and the ratio of FSH to LH were significantly decreased in COVID-19 patients (Ma et al., 2020).

This might be the first direct evidence for the influence of COVID-19 on testicles’ ability to produce sex hormones; however, the results of this study should be followed by a more direct analysis of the seminal fluid of COVID-19 patients to evaluate the effect—if any—on sperm count, volume, morphology or motility. It has been reported that SARS-CoV causes orchitis in addition to other complications (Xu et al., 2006), so it is also possible that SARS-CoV-2 may cause the same complication in males.

Y NO DO THIS ON JABBEES?

And it may kill pregnant women only:

Pregnant women have been shown to be at high risk of comorbidity and mortality related to influenza infections (Rasmussen, Jamieson, & Bresee, 2008; Rasmussen, Jamieson, & Uyeki, 2012). The previous SARS infection showed that pregnant women had higher fatality rate (25%) compared to the general population (10%; Wong et al., 2004). With the rise of numbers of pregnant women and children affected by COVID-19, it is worth to know if pregnant women are a high-risk group for COVID-19 death or increased hospitalisation and also to evaluate the risk of vertical transfer either from the mother to the foetus or from the neonates to the mother.

Neonatal health is another important concern in the COVID-19-infected mothers. In a study from Wuhan, 33 neonates were born to mothers with COVID-19, and no health complications were reported except for shortness in breath in four cases (Zeng et al., 2020). Other studies, including less number of cases, did not report any neonatal health issues except for low birthweight (<2,500 g) and premature delivery (Cao et al., 2020; Chen & Lou, 2020). Two other studies from China and Iran reported two neonatal deaths out of 19 cases studied (Hantoushzadeh et al., 2020; Zhu, Wang, et al., 2020). No cases of miscarriages have been reported in the first trimester of COVID-19 pregnancies. Overall, it seems that neonates delivered by COVID-19 pregnant mothers have no increased risk of clinical complications compared to normal pregnancies and some of the reported neonatal complications could be related to mothers’ overall health status rather than a consequence of COVID-19 infection.

Then why jab them?

The risk of vertical transfer of SARS-CoV-2 between the mother and the foetus is possible knowing that the ACE2 receptor is expressed in the placenta and uterus (Levy et al., 2008); however, most published data do not support this predication as most neonates born for mothers affected by COVID-19 tested negative (Chen et al., 2020; Liu et al., 2020; Yu et al., 2020). A few studies have reported a vertical transfer of SARS-CoV-2 from the mother to the neonates (Hantoushzadeh et al., 2020; Yu et al., 2020), but these studies should be carefully interpreted as they occur less frequently and possibly resulted because of the neonatal exposure to SARS-CoV-2 after delivery.

One way to get you on the hook financially is reproductive tech.

Risk of ovarian hyperstimulation syndrome should be taken very seriously during COVID-19 pandemic crisis and all guidelines clearly stated that reproductive endocrinologists should adopt gonadotropin-releasing hormone (GnRH) antagonist as a default protocol for ovarian stimulation with GnRH-agonist trigger to minimise the risk of ovarian hyperstimulation syndrome (OHSS), hospital admissions and intensive care unit (ICU) occupancy (ASRM; Carugno et al., 2020ESHREJSF).

Isn’t that an endometriosis fertility treatment? Odd. So you’re saying it works?

Many health issues related to COVID-19 have been addressed in this review. Pregnancy and maternal health have been discussed. Many reports have evidences against a direct link between COVID-19 and maternal death. Neonates born to a COVID-19 mothers are not at increased risk of adverse health consequence compared to the ones born for COVID-19-unaffected mothers, and the possibility of viral vertical transfer has not been confirmed. Large cohort studies should be followed to confirm these results; additionally, first-trimester COVID-19 cases should be included and be evaluated for the risk of miscarriages.

The gender difference in COVID-19 incidence, comorbidity and death rates—males are at higher risk—requires prompt actions to understand the source of difference biologically and behaviourally. Viral infection by HPV, HSV, HIVs, HBV, HCV and MuV challenges reproductive health and can be considered as a risk factor for male infertility. These viruses have been detected in semen and can impair testicular function. Some viruses such as HIV, MuV and SARS-CoV are associated with orchitis resulting in male infertility, so it would be interesting to study if SARS-CoV-2 can cause the same problem. Because many males at childbearing age are affected by COVID-19, the high expression of ACE2 receptor in the testes and the association of COVID-19 with fever; a multidimensional andrological translational research project was suggested (Salonia et al., 2020). This project aims to develop international collaboration for data registry, hormonal studies and genomic studies to better understand the sex difference for COVID-19 health-related consequences.

re the endo treatment


GnRH agonists are a group of drugs that have been used to treat women with endometriosis for over 20 years [1]. They are modified versions of a naturally occurring hormone known as gonadotropin releasing hormone, which helps to control the menstrual cycle.

At present, the usual length of treatment with a GnRH agonist is 3–6 months. However, in Germany, 12 months treatment with add-back therapy (5 mg of norethisterone per day) has been approved, and other countries may do the same in the future.

Covid spike protein damages heart paper

Water is also wet.

https://www.biorxiv.org/content/10.1101/2020.12.21.423721v1

The SARS-CoV-2 spike protein disrupts the cooperative function of human cardiac pericytes – endothelial cells through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease

paper DECEMBER 2020

AKA they KNEW

(they knew and they pushed it on you – and your kids, soon!)

Findings We show, for the first time, that the recombinant S protein alone elicits functional alterations in cardiac PCs. This was documented as: (1) increased migration, (2) reduced ability to support EC network formation on Matrigel, (3) secretion of pro-inflammatory molecules typically involved in the cytokine storm, and (4) production of pro-apoptotic factors responsible for EC death. Furthermore, the S protein stimulates the phosphorylation/activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) through the CD147 receptor, but not ACE2, in cardiac PCs.

Accordingly, the neutralization of CD147, using a blocking antibody, prevented the activation of ERK1/2 and partially rescued the PC function in the presence of the S protein.

SO do they permit this treatment to their loyal pets?

I think you’ll find the storms fully operational by the time flu season arrives. AKA Coof Coof Part Two. Satanist humour is killing everyone scared enough of death to get guinea pigged. Great way to sort wheat from chaff actually.

Interpretation Our findings suggest the new, intriguing hypothesis that the S protein may elicit vascular cell dysfunction, potentially amplifying, or perpetuating, the damage caused by the whole coronavirus. This mechanism may have clinical and therapeutic implication.

TECHNICALLY, EVERYONE DIES FROM HEART FAILURE.

TECHNICALLY.

which is the best kind of correct

allow me to un-memoryhole a meme

ANOTHER!

CBA, tbh
watch Black Books, I bid thee

First autopsy of a jabbed corpse

Almost every organ had high levels, almost. Almost total infestation. Almost like someone injected it!

Boosters push and more explained at bottom.

“The first-ever postmortem study of a patient vaccinated against COVID-19 has revealed that viral RNA was found in every organ of the patient’s body, meaning that the vaccine is either ineffective or the coronavirus actually spreads faster in vaccinated individuals.”

Both. But more Latter. And more fatal. I already covered the jabbed dead versus normal. Jabbed are literally more likely to die from it. MSM is hiding this and going on about symptoms. Dead people have reduced symptoms, can confirm.

paper here

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8051011/

“A previously symptomless 86-year-old man received the first dose of the BNT162b2 mRNA COVID-19 vaccine. He died 4 weeks later from acute renal and respiratory failure. Although he did not present with any COVID-19-specific symptoms, he tested positive for SARS-CoV-2 before he died. Spike protein (S1) antigen-binding showed significant levels for immunoglobulin (Ig) G, while nucleocapsid IgG/IgM was not elicited. Acute bronchopneumonia and tubular failure were assigned as the cause of death at autopsy;

however, we did not observe any characteristic morphological features of COVID-19.

Postmortem molecular mapping by real-time polymerase chain reaction revealed relevant SARS-CoV-2 cycle threshold values in all organs examined (oropharynx, olfactory mucosa, trachea, lungs, heart, kidney and cerebrum) except for the liver and olfactory bulb. These results might suggest that the first vaccination induces immunogenicity but not sterile immunity.”

So to save 86 year-olds, for like, six months, we need to damage all young adults and children? Fucking locusts. Are the Bad Boomers in power pushing this a Biblical plague? Maybe the jab itself is more Boomer Doomer than the wild virus.

It makes sense the liver would be clear because the liver’s function is clearing that shit but finding it in the heart? Goner. Dead man walking. Kidney? Suggests liver moved it there. Cerebrum? Yep, zombie.

Maybe the liver pushed it out of the liver, and back into the bloodstream, infecting the brain?
Old people and some heavily disease-burdened (like STDs) have thin blood brain barrier.

Definition:

The cerebrum or telencephalon is the largest part of the brain containing the cerebral cortex, as well as several subcortical structures, including the hippocampus, basal ganglia, and olfactory bulb. In the human brain, the cerebrum is the uppermost region of the central nervous system.Wikipedia

Brain damage.

All we need is psychosis and they’re literal zombies. Maybe the psychotic break happens later, once it’s really stewed in the brain juices for a while. It’s written off as dementia in old people so may already be happening. Maybe they get a form of terminal agitation in addition. I do actually know my stuff. When it’s in the basal ganglia you are absolutely screwed. That’s motor control. It’s in the hippocampus possibly explaining the terminally stupid decision to get a second one. It’s damaging memory then, which suggests senility symptoms oncoming. I wonder if it’s more likely to kill small or large amygdala people faster. Likely smaller.

What is the overall effect of this death stick? Advanced cellular senescence? Meaning the average age of death would be those with least lifespan left, presently seen, but that will just keep getting younger and younger and younger. Logan’s Run modRNA mod? So a basic model we assume their remainder lifespan is cut in half.
Does this help pension plans and national debt?
Well assuming 80 is lifespan (slightly shorter in men, who are dying faster from this…)
then a 60yo would die at 70,
a 50yo would die at 65,
a 40yo at 60,
a 30yo at 55,
a 25yo at ~50.
a 20yo at <50,
a 10yo at 45
a 5yo at 40 … etc. Down to school age.

Nobody would die before 35 except anomalies. Do we see this? Why try to deny those unless pattern?

Anomalous deaths would be acute advanced senescence. Intention may be largely chronic.
They can blame global warming.

So, yes. That’s very neat. A lot of younger fertile people getting it would die around menopause/manopause. Hence, perfect economic efficiency is achieved. The aging (genetic void) population dies off as soon as reproduction is achieved. We’d need at least ten years to see if average lifespan has gone down (80 to 70). Assuming this simple model. Younger Boomers and Gen Xers are the ones to watch. A reversal of lifespan is unprecedented. This is the slowest kill model and explains the push until 2023*. We’ll begin to notice by then en masse. This is why new techs need a decade PLUS of human trials. They look at lifespan.

*MPs love the book Nudge.
Has the NHS guaranteed treatment for genomic ‘vaccine’ damage? No. Nobody is talking about this.
Experimental subjects are considered consenting adults, so may not be eligible for NHS treatment.

Add in a sterilising effect especially in men, STD transmission, and the guidestones would be about right.

If that basic of the most basic models is correct, then the kids currently injected will die shortly after their feckless parentals.
Remember, saving the NHS also means fewer old people burdening it like lampreys. They could come out later and thank you for your willing participation, since you did technically save the NHS – by dying younger.
Experiments are permitted to legally deceive you, so long as they debrief you. In 2023.

By accelerating aging population, that’s very eugenic technically but deeply wrong re family. Surplus of orphans. Pedo paradise. Adult IQ would be higher (and GDP shoot up) since the morons would’ve happily skipped along for the euthanasia, children in tow.

The average age is 80-something now because they have no remainder, so it becomes weeks, not years. It fits.

And there’s no known time limit on shedding those synthetic SPs, secondhand smoke-like. At a certain uptake, society may be fumigating itself. Birth rates already have tanked. We may need a leper colony. They could be lifelong biohazards. They could easily test their exhalation at different points post-experimental injections. PE majors have a tube you breathe into, they could easily do it. The fact they don’t means they know the result would make them hated. Could be like the Island 2005 film.

Meanwhile

The basal ganglia are a group of subcortical nuclei, meaning groups of neurons that lie below the cerebral cortex. The basal ganglia is comprised of the striatum, which consists of the caudate nucleus and the putamen, the globus pallidus, the subthalamic nucleus, and the substantia nigra The basal ganglia are primarily associated with motor control, since motor disorders, such as Parkinson’s or Huntington’s diseases stem from dysfunction of neurons within the basal ganglia. For voluntary motor behavior, the basal ganglia are involved in the initiation or suppression of behavior and can regulate movement through modulating activity in the thalamus and cortex. In addition to motor control, the basal ganglia also communicate with non-motor regions of the cerebral cortex and play a role in other behaviors such as emotional and cognitive processing.

If it retarded them, I doubt any of us would notice.

An earlier coronavirus vaccine paper: why boosters and well, all of this really

https://pubmed.ncbi.nlm.nih.gov/14676007/

Vaccines against infectious bronchitis of chickens (Gallus gallus domesticus) have arguably been the most successful, and certainly the most widely used, of vaccines for diseases caused by coronaviruses, the others being against bovine, canine, feline and porcine coronaviruses. Infectious bronchitis virus (IBV), together with the genetically related coronaviruses of turkey (Meleagris gallopovo) and ring-necked pheasant (Phasianus colchicus), is a group 3 coronavirus, severe acute respiratory syndrome (SARS) coronavirus being tentatively in group 4, the other known mammalian coronaviruses being in groups 1 and 2. IBV replicates not only in respiratory tissues (including the nose, trachea, lungs and airsacs, causing respiratory disease), but also in the kidney (associated with minor or major nephritis), oviduct, and in many parts of the alimentary tract–the oesophagus, proventriculus, duodenum, jejunum, bursa of Fabricius, caecal tonsils (near the distal end of the tract), rectum and cloaca (the common opening for release of eggs and faeces), usually without clinical effects. The virus can persist, being re-excreted at the onset of egg laying (4 to 5 months of age), believed to be a consequence of the stress of coming into lay. Genetic lines of chickens differ in the extent to which IBV causes mortality in chicks, and in respect of clearance of the virus after the acute phase. Live attenuated (by passage in chicken embryonated eggs) IBV strains were introduced as vaccines in the 1950s, followed a couple of decades later by inactivated vaccines for boosting protection in egg-laying birds. Live vaccines are usually applied to meat-type chickens at 1 day of age. In experimental situations this can result in sterile immunity when challenged by virulent homologous virus. Although 100% of chickens may be protected (against clinical signs and loss of ciliary activity in trachea), sometimes 10% of vaccinated chicks do not respond with a protective immune response. Protection is short lived, the start of the decline being apparent 9 weeks after vaccination with vaccines based on highly attenuated strains. IBV exists as scores of serotypes (defined by the neutralization test), cross-protection often being poor. Consequently, chickens may be re-vaccinated, with the same or another serotype, two or three weeks later. Single applications of inactivated virus has generally led to protection of <50% of chickens. Two applications have led to 90 to 100% protection in some reports, but remaining below 50% in others. In practice in the field, inactivated vaccines are used in laying birds that have previously been primed with two or three live attenuated virus vaccinations. This increases protection of the laying birds against egg production losses and induces a sustained level of serum antibody, which is passed to progeny. The large spike glycoprotein (S) comprises a carboxy-terminal S2 subunit (approximately 625 amino acid residues), which anchors S in the virus envelope, and an amino-terminal S1 subunit (approximately 520 residues), believed to largely form the distal bulbous part of S. The S1 subunit (purified from IBV virus, expressed using baculovirus or expressed in birds from a fowlpoxvirus vector) induced virus neutralizing antibody. Although protective immune responses were induced, multiple inoculations were required and the percentage of protected chickens was too low (<50%) for commercial application. Remarkably, expression of S1 in birds using a non-pathogenic fowl adenovirus vector induced protection in 90% and 100% of chickens in two experiments. Differences of as little as 5% between the S1 sequences can result in poor cross-protection. Differences in S1 of 2 to 3% (10 to 15 amino acids) can change serotype, suggesting that a small number of epitopes are immunodominant with respect to neutralizing antibody. Initial studies of the role of the IBV nucleocapsid protein (N) in immunity suggested that immunization with bacterially expressed N, while not inducing protection directly, improved the induction of protection by a subsequent inoculation with inactivated IBV. In another study, two intramuscular immunizations of a plasmid expressing N induced protective immunity. The basis of immunity to IBV is not well understood.

Serum antibody levels do not correlate with protection, although local antibody is believed to play a role.

Adoptive transfer of IBV-infection-induced alphabeta T cells bearing CD8 antigen protected chicks from challenge infection. In conclusion, live attenuated IBV vaccines induce good, although shortlived, protection against homologous challenge, although a minority of individuals may respond poorly. Inactivated IBV vaccines are insufficiently efficacious when applied only once and in the absence of priming by live vaccine. Two applications of inactivated IBV are much more efficacious, although this is not a commercially viable proposition in the poultry industry.

However, the cost and logistics of multiple application of a SARS inactivated vaccine would be more acceptable for the protection of human populations, especially if limited to targeted groups (e.g. health care workers and high-risk contacts). Application of a SARS vaccine is perhaps best limited to a minimal number of targeted individuals who can be monitored, as some vaccinated persons might, if infected by SARS coronavirus, become asymptomatic excretors of virus, thereby posing a risk to non-vaccinated people.

Looking further into the future, the high efficacy of the fowl adenovirus vector expressing the IBV S1 subunit provides optimism for a live SARS vaccine, if that were deemed to be necessary, with the possibility of including the N protein gene.

Nanolipids gather in ovaries, adrenals and liver

Imagine my shock.

https://jnm.snmjournals.org/content/54/11/1996

“We have documented the pharmacokinetics and biodistribution of lipidots, synthetic 55-nm-diameter lipid nanoemulsions with potential applications for diagnostics and drug delivery. After intravenous injection in healthy mice, lipidots are stable in blood and taken up preferentially in liver, adrenals, and ovaries, where they release their lipidic cargo. Lipidots depict an original biodistribution, not previously reported for other inorganic or organic nanoparticles, toward organs involved in steroid hormone synthesis and storage (adrenals and ovaries) and localize to precise sites in these organs, suggesting potential applications for imaging and drug delivery.”

The nanolipids are the modRNA carrier. So where lipids go… I think we have our organ sequester, gentlemen.
NLs are in at least the moderna and Pfizer ‘vaccines’.
https://portal.ct.gov/-/media/Coronavirus/Community_Resources/Vaccinations/Print-Materials/Fact-Sheets/Ingredients_English.pdf

A friend suggested the Pfizer one may be ‘safe’ because rich areas are buying it. That was Boomers avoiding the heart effects reported from AZ, possibly to push them to the others, none of them are safe.
Potassium is also used in lethal injections, to stop the heart. It’s in Pfizer. Talk about red herring. Watch deaths from heart disease in, say, the next three years.

In this country, they don’t give you even the illusion of choice, it’s largely based on age and supposed availability. There is no safe one.

The lipids preferentially allow the modRNA to ‘slip into the cell’ of those organs, as the enclosed PDF plainly states.

nb The effects described in Malice or Mistake? in the brain are prionlike, they needn’t be actual prions.

Social anxiety aka Wanker’s Syndrome

In this studythis study, and this study, it was found that people who were extroverts, outgoing and social had more D2 receptors in their brain (this is an oversimplification of the results. Link is provided for more detailed read.

It has been shown through the science of addiction and fMRI scans that the brain chemistry of the porn addict mimics the brain chemistry of addicts with other forms of addiction. These brain chemistry are characterized by hypofrontality (memory and cognitive impairment) and largely reduced number of D2 Receptors.

Actually, hypofrontality is a nice way of saying retardation since it refers to incomplete development or function. That’s literally what a retard is, the word meaning slow in French.

So they are literally retarding themselves, the wankers.

re d2

https://pubmed.ncbi.nlm.nih.gov/8033754/

COMMENTS: First study to show that drug use causes a decline in dopamine (D2) receptors. Important because addicts have a low number of such receptors, which may contribute to addiction. Also shows that receptors can bounce back, but rate is highly variable and not related to baseline D2 receptors.

https://link.springer.com/article/10.1007/s00439-012-1145-7

Public pensions reduce fertility

https://pubmed.ncbi.nlm.nih.gov/1213215/

Socialism kills. All Marxism is anti-natal, it’s the only thing it has in common.
Hence, national socialism is fucking retarded, sorry. It doesn’t work. You can’t have a half-evil system. It makes people lazy, as we see:

A number of population scholars have asserted that social security programs such as old-age programs lead to decreased fertility levels because parents need not rely on children for “security” in old age. There is, however, a paucity of empirical data on the above. This paper analyzes 67 countries and shows that social security programs have a measurable negative effect on subsequent levels of fertility.

This might go down in history as the thing to doom the Boomers, demographically.

In fact, the social security programs appear to have as much of an independent impact on fertility as do the traditional correlates of fertility (infant mortality, education and per capita income).

Explains the sheer drop in fertility in places like Poland, and why places like Russia and China are currently bricking it.

Then you have fake Catholics like the French, fucking around and never marrying because there’s no stigma any longer. Socialism preserves a husk of civilization while hollowing out the core.

It’s popular for insecure morons to say higher education should be banned but it replaces ballrooms for the high IQ to meet one another. Education is K-select, that’s why Marxists have tried to destroy it. Would you rather they screw the local waitress and have dipshit kids? On your tax bill? Assortative mating must be enabled for a healthy, functioning society. Ban foreign students and there’s more room by far. Then you don’t have national security risks like the Chinese stealing missile data AMERICA.

College educated parents (yes, both) have higher IQ children. The right wing gets triggered over this and other facts where the universe doesn’t revolve around men (or women, but they don’t care there). As covered previously, most child IQ is inherited maternally. So we know it’s men to blame for fucking the dumb broads, who exhibit sexual selection like a leech being discerning in a blood bank. Stop fucking stupid women. At least, don’t be surprised when the kids are entitled douchebags. If your kids are stupid, and you think it isn’t you – it’s your choice of woman.

Ancient European DNA

Once more, I implore and painstakingly EXPLAIN, IF they can breed, they are, by DEFINITION, the SAME species.

http://www.cell.com/current-biology/fulltext/S0960-9822(21)00592-3

Different race? Maybe. Same species? Definitely.

Peştera Muierii woman is related to Europeans, but she is not a direct ancestor

Doesn’t have to be, a lot of bloodlines died.

Reduced diversity in Europe caused by Last Glaciation, not out-of-Africa bottleneck

Natural selection kills diversity. We know this.

Genetic load appears indifferent across 40,000 years of European history.

Postmodern habits like drugs, drinking, bad diet, sleeping around, can screw up your epigenetics over a few generations. We absorb viruses into our genome. Outbreeding depression does it in one. You can, in fact, fuck up tens of thousands of years of effort on part of your ancestors. If only we had a commandment about this.

Pet theory: planes are evil. Sink the boats.

Few complete human genomes from the European Early Upper Palaeolithic (EUP) have been sequenced. Using novel sampling and DNA extraction approaches, we sequenced the genome of a woman from “Peştera Muierii,” Romania who lived ∼34,000 years ago to 13.5× coverage. The genome shows similarities to modern-day Europeans, but she is not a direct ancestor. Although her cranium exhibits both modern human and Neanderthal features, the genome shows similar levels of Neanderthal admixture (∼3.1%) to most EUP humans but only half compared to the ∼40,000-year-old Peştera Oase 1. All EUP European hunter-gatherers display high genetic diversity, demonstrating that the severe loss of diversity occurred during and after the Last Glacial Maximum (LGM) rather than just during the out-of-Africa migration. The prevalence of genetic diseases is expected to increase with low diversity; however, pathogenic variant load was relatively constant from EUP to modern times, despite post-LGM hunter-gatherers having the lowest diversity ever observed among Europeans.

The Neanderthals were human. They were, at most, a race. Basic classification 101. It’s politically incorrect to admit this.

Welcome Global Cooling, it kills off redundant diversity. The people still living are the winners.

OOA is laughable at this point. Multi-Regional is correct. They don’t have to keep tweaking it to fit the data, replete with Black Swans that shouldn’t be there.

Assumption is incorrect, diseases become more serious, the higher the diversity. It’s akin to mixing random chemicals in a beaker. You’re more likely to blow your arm off, the more different the ingredients or elements. Well, mutations work the same way and most are disadvantageous i.e. they lower Darwinian fitness. A novel combination is dangerous. Inbreeding depression takes centuries in a super-restricted, incestuous environment; meanwhile, outbreeding depression occurs in one generation between any two genomes of sufficient distance. Odds are, if a kid has some super-rare obscure disease, barely recorded, they’re mixed race. The more mixed, the more health problems, including mental health. Taboos are based on health outcomes. They demonstrate low fitness for any one environment and ‘fail to thrive’ in either parental environment as a result. It dooms them to never belong and fit in, a core human need as a social species. Every group has a runt to its litter, but that shouldn’t be encouraged as the norm, it’s cruel. Happily, this means such mutants and feeble specimens were almost unheard of throughout our history, so we have nothing to feel guilty about. It’s literally the parent’s fault they made an experimental kid. Nobody forced you to play God.

This is why Africans in Africa are healthier than the mongrels in America. It isn’t just diet. Also why full-blooded Africans generally hate them. They are equally disgusted by the degeneration as any other race, it’s human aversion to disease.

Similarly, White Americans have extremely high white DNA but also suffer poorer health compared to their homelands. Why? Admixture of subrace. The same applies to a lesser-degree within a race, of sufficient genetic distance. It’s unlikely to be fatal, but breeding with a person with high mutations (r-type) will ruin the bloodline of the person whose is low. It’s only fine if they’re both low, which is unlikely when so distant in ancestry as to cross countries (and emigration is r-select). Consider the children of supermodels. Regression to the mean, except mutations only build. So you get a bland, dull looking child, nothing special. Breeding two racehorses is fine, breeding it with a donkey makes a mule, however good the racehorse genes of one parent. That’s the evil of genetic regression. Beware it. A racehorse with a regular horse may be fine but is likely to be uninspiring by the racing parental standard. This also applies to plants and flowers. Excess distance causes fertility dysfunction and is collectively called the process of speciation. Enough of the odd couples die off genetically while others, more natural, succeed and replace them using natural selection (by omission) to win zero sum. It works on a mathematical level. It’s basic game theory. Live or die.

EVOLUTION HAS NO CONTINUOUS SPEED. IT IS AN ONGOING PROCESS AND OPERATES FASTER SOME TIMES THAN OTHERS. I repeat, evolution is non-uniform as a biological driving force to live. I’ve never seen a shred of proof for it being the same everywhere, at all times and in all peoples. That smacks of absurd equalism and doesn’t account for the violence of history, both natural disasters and wars. There is much to the contrary, like this. Bloodlines die out, in part, all the damn time. All the bloody time! Yet certain people who claim to be high IQ like to pretend it has a constant speed like ‘c’, it is a positive claim and I’d like evidence. It doesn’t have to make sense to you, to be demonstrably true.

How many of Edison’s many children survived? Surprisingly few. That’s in a century. Writ large, same pattern. The birth rate doesn’t matter, longevity of genes does. Do not conflate them. Dilution is also a partial death. It’s like genetic atrophy. When children disappoint their parents, whose fault is that?

I find it funny supposed Christians mock evolution, only to insist on muh birth rates. If you believe in Revelations, it won’t matter, because winning is Darwinian. It isn’t about cross-comparisons to other groups, more r-select (read: arrogant while times are good) and their over-populating to over-consume and eventual, frequent famine (hello China), but quality within. Genetics are moreso about what you DON’T have than what you do. i.e. You can’t steal IQ, China, keep funding genetic engineering though. You tried. R-types can only run an ‘Empire’ of inferior quality by oppressing their own kind and even then, it fractures and implodes due to their sadism (low group loyalty > no in-group empathy). They are collectivists who hate freedoms and rights. Introduce more k-select competition and they’re easily brought to heel, like the French. Beaten (and saved) by a nation of shop-keepers. There’s a difference between conspicuous consumption and responsible innovation. R-types can’t tell until it’s all failing and none of their people running the machines (high corruption, nepotism) were smart enough to invent them (low child investment), so cannot fix it. Corrupt societies deserve to suffer and die. Evolution is social as much as genetic. = epigenome

TLDR: With debt bubbles as with population bubbles. It’s the same bubble. Malthus wins.

While K-types look foolish during good times, they lose the least (high child investment pays off) when times get tough and due to high group loyalty, fare better against challenges by more r-groups. Ks have the steadier gene = winning. You don’t buy a Ferrari on credit to compete with your neighbour, you wait for his to get repossessed.

See: Skyscraper Index. Recently: Asian.

This low load of mutations and high fertility into the modern era, suggests Neanderthals were the same race, and they’re trying to report the finding without admitting this. Curse the editors.

nb I wonder whether the RNA trial mutants will be having fertility problems with their own, or only with the rest of us. Speciation is epigenetic.

RNA can be written into DNA

Imagine my shock.

Pause. Wait. Imagine it.

Imagine my shock.

“This work opens the door to many other studies that will help us understand the significance of having a mechanism for converting RNA messages into DNA in our own cells,” says Richard Pomerantz, PhD, associate professor of biochemistry and molecular biology at Thomas Jefferson University. “The reality that a human polymerase can do this with high efficiency, raises many questions.” For example, this finding suggests that RNA messages can be used as templates for repairing or re-writing genomic DNA.

The work was published June 11th, 2021, in the journal Science Advances.

Except we knew this for ages and I’d posted about it before, this just proves it further.

Well duh, messengers don’t just go ONE way?

It’s all part of your epigenome, I explained this before.

Together with first author Gurushankar Chandramouly and other collaborators, Dr. Pomerantz’s team started by investigating one very unusual polymerase, called polymerase theta. Of the 14 DNA polymerases in mammalian cells, only three do the bulk of the work of duplicating the entire genome to prepare for cell division. The remaining 11 are mostly involved in detecting and making repairs when there’s a break or error in the DNA strands. Polymerase theta repairs DNA, but is very error-prone and makes many errors or mutations. The researchers therefore noticed that some of polymerase theta’s “bad” qualities were ones it shared with another cellular machine, albeit one more common in viruses — the reverse transcriptase. Like Pol theta, HIV reverse transcriptase acts as a DNA polymerase, but can also bind RNA and read RNA back into a DNA strand.

DNA polymerase, there’s a term to tuck in your belt.

“Our research suggests that polymerase theta’s main function is to act as a reverse transcriptase,” says Dr. Pomerantz. “In healthy cells, the purpose of this molecule may be toward RNA-mediated DNA repair. In unhealthy cells, such as cancer cells, polymerase theta is highly expressed and promotes cancer cell growth and drug resistance. It will be exciting to further understand how polymerase theta’s activity on RNA contributes to DNA repair and cancer-cell proliferation.”

RNA-mediated DNA repair. Quite an arse covering.

If it can repair, it can damage.

When highly expressed, the process promotes cancer growth? Really? Fascinating. I’ll await the RNA trial results from the control group of organic humans with interest. Extreme interest.

The drug resistance is interesting, that wouldn’t include anti-virals, would it?
To people with tainted RNA, would transcriptase be a kill shot?

Here’s hoping my idiotic relatives don’t shed on me into mutantdom. If they do, I’ll tell you.

UN population paper to 2300

I think I’ve posted this before and I know I’ve recently spotlighted the dying demographic nations like Poland (lowest fertility rate in the EU).

But let’s look again and wonder how such steep changes could happen, shall we?

“Population growth in Eastern Europe is now negative, and Southern Europe is projected to join it with zero growth around 2005.

Western and Northern Europe, in contrast, are expected to maintain positive growth until around 2025 and 2040, respectively (figure 36). Declines in growth not only come earlier but are also much sharper in Eastern and Southern Europe than in Western and Northern Europe. Were international migration eliminated, zero growth in Western and Northern Europe would come instead much earlier, around 2005. With no migration, the growth trajectories for Western, Northern, and Southern Europe would still be roughly similar but would be pegged at a lower level, but the growth trajectory for Eastern Europe would be little changed. Looking beyond 2050, one sees each region return gradually to zero or slightly positive growth.”

But by all means think voting and anti-marriage propaganda will help…. It’s like demographic Santa. Babies can be wished into existence! What incentives?
Also, EE, this is why you don’t traffic and pimp out your nubile young women to rich Arabs and STD-ridden tourists. You ate the demographic seed crop. If you continue to betray your women (fact: most white people are women) then you deserve to die out. Misogyny (as with misandry) are anti-natal. Figure 35 shows the wages of sin is death i.e. treason = extinction. The MRA/MGTOW anti-natal propaganda is largely the rejected gamma trying to genetically murder those above him (the coward’s way, Wormtongue) by fish bicycle logic. Surely you’re smarter than that? SJWs perform the same gamma/spiteful mutant function among women.

The United Kingdom dominates Northern Europe demographically, with 64 per cent of regional population. Its growth trajectory is about 0.1 points higher than that for Northern Europe as a whole. The region also includes three small Baltic countries with economies in transition: Estonia, Latvia, and Lithuania. Their growth trajectories are radically different, being even more negative than that for Eastern Europe. The remaining European countries with economies in transition are all in Eastern Europe, except for Albania and the successor states to Yugoslavia, which are in Southern Europe. However, growth in Albania and the former Yugoslav republics is not that different from, and actually slightly higher than, growth in Southern Europe as a whole. Southern Europe is dominated by Italy and Spain, whose projected slow growth is reflected in the regional trajectory.”

Those whom the gods wish to destroy, they first make mad. Reprobate mind? Sexually decadent cultures?

“Projected fertility trends are consistent with the growth trends. Some initial fertility decline further below replacement is expected in this decade, except in Western Europe, where fertility is believed to have hit bottom in the early 1990s and has risen slightly since then (figure 38).” That’s Labour immigration policy.

Each region is then assumed to reach total fertility of 1.85 by 2045-2050, with Northern and Western Europe progressing along a higher trajectory than Southern and Eastern Europe. Within the following quarter century, fertility is then expected to rise further to replacement level, with Southern Europe lagging behind the other regions.”

Yet I find it hilarious that Eastern Europe is taking the most degenerate of white trash immigrants, the PUAs. They’ll soon learn it isn’t even race of the immigrant, it’s whether they’ll render your local population infertile with STDs and cause local disruption with their carousing. Like the Vikings, they’ll take your women. It’s the rule. And if the local women refuse, like Taharrush, they’ll be forced. I’d expect druggings to become commonplace (including alcohol spikings) whenever PUAs move into an area.

Sort your incitement to rape laws NOW. Protect your culture. Don’t become like NY or London. Do not let the sexual locusts eat your nubile seed crop. r-types emigrate.

“Fertility stays at current levels in the constant projection scenario, which leads to incredibly large numbers for world population. For the European population, however, it leads instead, in the long run, to startlingly low numbers. By 2300, Western, Southern, and Northern Europe would each have only 28-30 million people, and Eastern Europe
would have only 5 million.
The European Union,which has recently expanded to encompass 452-455 million people (according to 2000 or 2005 figures) would fall by 2300 to only 59 million.
About half the countries of Europe would lose 95 per cent or more of their population, and such countries as the Russian Federation and Italy would have only 1 per cent of their population left. Although one might entertain the possibility that fertility will never rise above current levels, the consequences appear sufficiently grotesque as to
make this seem improbable.”

95 per cent or more of their population

and party countries like Italy and the world’s strip club Russia:

only 1 per cent of their population left

“sufficiently grotesque” is code for effective genocide folks

Also: You don’t judge whether something is POSSIBLE by emotional appeal.

See, you don’t need to kill everyone, just most of them, to prevent a functioning economy, especially the young people, and if you can keep them bachelors so much the better, because white people need to marry first before they breed. Distractions include careerism, the gym and notch counting.

“These changes take a century. Quicker societal adjustments are necessary when demographic change is rapid in the short-run, though such demographic changes tend to be more difficult to predict. Table 9 shows the highest and lowest growth rates expected for each country in any period between 2000 and 2300. Most of the largest positive growth rates appear in 2000-2005, while fertility is still high in various countries. The largest negative growth rates appear close to 2050 or beyond 2100, when countries enter a period of below-replacement fertility. European countries tend to show slowest growth earlier, African countries later, except for some Southern African countries where slow growth appears around 2020-2030 because of HIV/AIDS.”

or a SARs bioweapon.

Yet the anti-natal channels on Youtube are the only kind exempt from the so-called ‘redpill’ ban hammer.

Makes ya think. Activates the almonds. Rustles my jimmies. I wonder (((why))). They hate white males and they’re telling them to nix their genome with the snip or race mixing. I wonder why those channels are up? Why are so many pick-up artists non-white? And yes, that includes the Jews. When do we get the AQ – the Asian Question of them inserting themselves into our culture and policies? Hello fellow hwyte male. Let them slice your balls.

That’s the Boomer fallout, the consequences of all the dysgenic policies, from abortion to the Pill to free love/hook-up/whoredom to Asian and African immigration/invasion. I know some of you didn’t vote for it, it still exists. I’ll be considered generationally along Trigglypuff so deal with it.

TABLE 8 is a sobering read.

e.g. Croatia, millions of population, -27 by 2100, maximum 0% change. Stop importing degenerates.

Israel 63M by 2100, curious. 70% + max change. Almost like they knew.

Poland -33M by 2100. By all means, let degenerates immigrate. Make it worse.

BY contrast, Somali 658 million. Not a typo.

Serbia, -26 million by 2100. Were the shekels worth it?

I’m sorry I base my opinions on data.

By comparison, so-called cucked Sweden minus 8 million by 2100.

So Eastern Europe is literally worse off than the Swedes. Nobody says anything. Controlled ops.

UK gains 10M, mostly non-Anglo, I’d wager. The native pop is suppressed by (economic) factors and anti-marriage propaganda.

America gains 53M, mostly mystery meat if you look at new births and white deaths. Thanks, Boomers.

Yemen gains 700M. Not a typo.

“In 2000-2005, 56 countries, out of 192, have total fertility of 4.0 or higher. By 2045-2050, the number will be zero. Instead, 139 countries will have total fertility under 2.0. Beyond 2050, however, the progression is not unilinear. The number of countries with fertility below 2.0 will fall, as more and more countries return to a replacement level just above 2.0. But fertility levels of 2.2 or higher are not expected to return.”

So Marxism of any kind (including precious socialists) will go the way of the dodo. The production simply won’t be there to leech from.

You read the rest. This century, the white man dies. If they endorsed anti-natal practices, it’s deserved. Revenge is mine, saith the LORD.

We need exogenic wombs, it seems. Because there won’t be enough fertile women to go around.

The races (sub-species) are biologically distinct and a study on ancient Africans

The races (sub-species) are biologically distinct, QED:
https://genomebiology.biomedcentral.com/articles/10.1186/gb-2002-3-7-comment2007

A debate has arisen regarding the validity of racial/ethnic categories for biomedical and genetic research. Some claim ‘no biological basis for race’ while others advocate a ‘race-neutral’ approach, using genetic clustering rather than self-identified ethnicity for human genetic categorization. We provide an epidemiologic perspective on the issue of human categorization in biomedical and genetic research that strongly supports the continued use of self-identified race and ethnicity.

Parroting a comment I made to Vox for SEO.

And just like white people have other ‘species’ DNA (Neanderthal), so too do Africans (non-Neanderthal).
https://phys.org/news/2011-09-modern-humans-interbred-archaic-hominin.html
I too, fucking love science.

“Instead, we looked at DNA from modern humans belonging to African populations and searched for unusual regions in the genome.”
And they were older than modern. Imagine my shock.
“What we do know is that the sequences of those forms, even the Neanderthals, are not that different from modern humans,” he said.
-BECAUSE THEY THE SAME SPECIES. Sorry, broke into spontaneous ebonics because of the topic.
“They have certain characteristics that make them different from modern DNA.”
No shit?

Could be better or worse depending on the variant. They refuse to clone Neanderthals because no company could own them (human rights are based on demonstration of human IQ) and they’d be the smartest human on the planet. It would show us all up. I want it to happen. Neanderthals were more civilized than us, we learnt funerary rites from them. Please clone the African ancestors too, see what happens.

“Then we asked ourselves what does the general pattern of variation look like in the DNA that we sequenced in those African populations, and we started to look at regions that looked unusual,” Hammer said. “We discovered three different genetic regions fit the criteria for being archaic DNA still present in the genomes of subSaharan Africans. Interestingly, this signature was strongest in populations from central Africa.”
I’ll fly high on this one and say no comment.

“We are talking about something that happened between 20,000 and 60,000 years ago – not that long ago in the scheme of things,” Hammer said. “If interbreeding occurs, it’s going to bring in a whole chromosome, and over time, recombination events will chop the chromosome down to smaller pieces. And those pieces will now be found as short, unusual fragments. By looking at how long they are we can get an estimate of how far back the interbreeding event happened.”
Outbreeding depression…. it isn’t inter-breeding, it’s out-breeding….
“We think there were probably thousands of interbreeding events,” Hammer said. “It happened relatively extensively and regularly.”

He can’t be saying, they were literally fucking monkeys? No. …No? No.
Are they technically humans they were screwing or not? At best, they mixed races. At worst, bestiality. I read a conspiracy that human anatomy is so weird because we’re the result of primates mating with hogs. That’s why pig hearts and such work on us. It was surprisingly detailed and I couldn’t think of anything to counter it.* I am also scared now.

I’m making the odd low/no effort post when I can be asked.

*Also explains the Biblical prohibition on pork.