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HPV vaccine-associated pathologies: Osteoporosis and cancer pathways - Part I
JUL 10

HPV疫苗相关的病理：骨质疏松和癌症途径 - 第一部分
7月10日

https://open.substack.com/pub/doorlesscarp953/p/hpv-vaccine-associated-pathologies

HPV vaccine-associated pathologies: Osteoporosis and cancer pathways - Part I
JUL 10

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Contents

1.0 Introduction

1.1 A nerve agent attack? Kind of
1.2 Human Papillomavirus (HPV)
2.0 Discussion

2.1 Viral oncogenic mechanisms
2.2 Osteoporosis
HPV vaccines
L1 protein binding to immune cells
Cytokine responses to HPV vaccines and cancer pathways
3.0 Parting shots

3.1 RSV deathshots™
3.2 Pharma share-apocalypse
3.3 Baffled health insurers
4.0 Concluding remarks

5.0 Disclaimer

6.0 References

1.0 Introduction

1.1 A nerve agent attack? Kind of

A relatively high incidence of chronic limb pain, frequently complicated by violent, tremulous involuntary movements, has been noted in Japanese girls following human papillomavirus vaccination.

The average incubation period after the first dose of the vaccine was 5.47 ± 5.00 months. Frequent manifestations included headaches, general fatigue, coldness of the feet, limb pain, and weakness.

The skin temperature of the girls with limb symptoms was slightly lower in the fingers and moderately lower in the toes. Digital plethysmograms revealed a reduced peak of the waves, especially in the toes.

Limb symptoms of the affected girls were compatible with the diagnostic criteria for complex regional pain syndrome.

The Schellong test identified a significant number of patients with orthostatic hypotension and a few with postural orthostatic tachycardia syndrome.

Electron-microscopic examinations of the intradermal nerves showed an abnormal pathology in the unmyelinated fibers in two of the three girls examined.

The symptoms observed in this study can be explained by abnormal peripheral sympathetic responses. The most common previous diagnosis in the patients was psychosomatic disease.

Recently, delayed manifestation of cognitive dysfunction in the post-vaccinated girls has attracted attention. The symptoms include memory loss and difficulty in reading textbooks and/or calculation.

From: “Neurologic Complications in HPV Vaccination” (2015)

Lewis Carroll Quote: “It's all in your head, Alice.”
1.2 Human Papillomavirus (HPV)

HPV belongs to the Papillomaviridae family of DNA viruses. It commonly infects the skin and mucous membranes of the body. There are more than a hundred types of HPV. Whilst most of these infections clear up harmlessly, some types of genital HPV may lead to neoplastic transformation, leading to cancer of the cervix. HPV has also been linked to cancers of the anus, penis, vagina, vulva, and the back of the throat (oropharyngeal cancer)¹.

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“Cryo-electron microscopy structure of the HPV type 16 viral capsid protein. Rendered from PDB: 5KEQ[112]”. By Opabinia regalis - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=80562689
From Wiki:

“Sexually transmitted HPV is divided into two categories: low-risk and high-risk. Low-risk HPVs cause warts on or around the genitals. Types 6 and 11 cause 90% of all genital warts and recurrent respiratory papillomatosis, which causes benign tumors in the air passages. High-risk HPVs cause cancer and consist of about twelve identified types.[11] Types 16 and 18 are responsible for causing most of the HPV-caused cancers. These high-risk HPVs cause 5% of the cancers in the world. In the United States, high-risk HPVs cause 3% of all cancer cases in women and 2% in men.[92]

Risk factors for persistent genital HPV infections, which increase the risk of developing cancer, include early age of first sexual intercourse, multiple partners, smoking, and immunosuppression.[1]”

This Substack will briefly discuss HPV-induced neoplastic transformation and the more commonly known HPV vaccine-related adverse events, but the main discussion is in support of a hypothesis — that both the virus and vaccinal proteins are associated with a significantly increased risk of pathologies, including osteoporosis, due to a sustained increased expression of pro-inflammatory cytokines. Immune priming helps to mediate the long-term effects observed.

I was prompted to investigate the pathology after citizen journalist The Underdog shared this anonymous post:

This work does not exclude the contribution of other vaccine-induced pathologies, such as premature ovarian insufficiency (POI)², which has been subject to various court cases and class actions. These included claims for osteoporosis, a heart condition, and POTS.

The burden of proof is high, and not in your favour.

(For information only, not an endorsement):

Our lawyers are helping victims who want to bring a Gardasil HVP vaccine lawsuit throughout the United States. Our law firm is particularly focused on ovarian failure cases that lead to infertility in women who have taken Gardasil in the last few years.

Gardasil is a vaccine intended to prevent human papillomavirus (HPV), which can sometimes lead to cervical cancer in women. Gardasil was developed by the embattled pharmaceutical company Merck & Co.

Merck obtained FDA approval for Gardasil in 2006 based on deceptive research and clinical trials that misrepresented the vaccine’s efficacy while concealing its safety risks and side effects. Merck then launched an aggressive and highly misleading marketing campaign to include millions of parents vaccinating their pre-teen daughters with Gardasil.

Filing a Gardasil lawsuit is not an anti-vax statement. A Gardasil vaccine lawsuit is a statement that this specific vaccine that we all assumed was safe might not be.

Gardasil settlement projections for different types of injuries
Gardasil Class Action Lawsuit Updates in 2025

April 25, 2025 – Appeal

Bellwether plaintiffs in the Gardasil vaccine MDL appealed multiple adverse rulings to the Fourth Circuit after Judge Bell dismissed most of their claims. The plaintiffs’ opening appeal brief is due May 27, 2025.

March 12, 2025 – Tough Ruling in MDL

The MDL judge in the Western District of North Carolina has ruled in favor of Merck, granting summary judgment on the grounds of implied preemption. The decision effectively blocks failure-to-warn claims brought by plaintiffs who allege that Merck should have included warnings about Postural Orthostatic Tachycardia Syndrome (POTS) and Primary Ovarian Insufficiency (POI) on the Gardasil label. There are other claims, but the reality is this is a failure to warn case. So it is a crushing blow in the MDL.

The court found that under federal law, Merck could not have independently added these warnings without FDA approval. Since the FDA has never required such warnings—and has consistently rejected claims that Gardasil causes POTS or POI—the court determined that state law failure-to-warn claims conflict with federal regulation and are therefore preempted. The ruling is a major victory for Merck in the federal litigation, as it eliminates one of the plaintiffs’ central legal claims.

The decision does not apply to state court cases. So while this ruling is significant, it does not end Gardasil litigation altogether. This decision applies only to cases consolidated in the MDL in federal court. State court lawsuits remain unaffected, and plaintiffs can still pursue claims under state law, particularly in jurisdictions where failure-to-warn claims are treated differently or where alternative legal theories—such as fraud, negligence, or design defect—are in play.

The contrast between state and federal litigation is already becoming apparent. A state court trial in Los Angeles, brought by a woman who alleges Gardasil caused a heart condition that left her in a wheelchair, was recently postponed due to concerns over potential jury bias. The delay stemmed from the confirmation of Robert F. Kennedy Jr. as U.S. Secretary of Health and Human Services. Kennedy, a long-time critic of vaccines, referred cases to a law firm handling Gardasil litigation and was set to financially benefit from some of these lawsuits before transferring his stake to his son. His highly publicized confirmation process led to concerns that jurors might be influenced by his vaccine-related advocacy.

So despite this federal preemption ruling, the broader fight over Gardasil is not over. State courts will continue to hear cases, and the legal battle over whether Merck adequately disclosed Gardasil’s risks will play out in those jurisdictions. Merck’s victory in the MDL means federal plaintiffs may now focus on other claims, such as fraud or design defect, while state court litigation remains active.

March 8, 2025 – Why Is Gardasil Not in Vaccine Court

Gardasil is covered by the VICP, which means individuals alleging harm from Gardasil must file claims in Vaccine Court before they can sue the manufacturer. However, Gardasil is not listed in the Vaccine Injury Table, which outlines specific injuries presumed to be caused by particular vaccines within a defined timeframe.

Because Gardasil is not on the table:

There are no presumptive injuries associated with it, according to the federal government (maybe Kennedy does something about this)
Claimants do not get the benefit of the legal presumption of causation.
They must prove, using medical records and often expert testimony, that the vaccine caused the injury.
Without the benefit of a table injury:

The burden of proof is higher.
Claimants must show that the vaccine “more likely than not” caused the injury (preponderance of evidence).
This often requires retaining expensive medical experts and assembling detailed scientific arguments.n.
More: https://www.lawsuit-information-center.com/gardasil-hpv-vaccine-lawsuit.html

2.0 Discussion

2.1 Viral oncogenic mechanisms

This is from a paper from 2002 by Hwang et al. “Human Papillomavirus Type 16 E7 Binds to E2F1 and Activates E2F1-driven Transcription in a Retinoblastoma Protein-independent Manner”³.

Lower-risk HPV types bind E7 protein less strongly to E2F1, a tumor suppressor. Strong binding helps higher-risk HPV to stop E2F1 from restricting cancer cell division:

The human papillomavirus (HPV) E7 oncoprotein can immortalize primary human cells and induce tumor formation. These properties of E7 depend on its ability to inhibit the activity of retinoblastoma protein (pRB), which in turn affects E2F function.
E2F proteins control the expression of genes involved in differentiation, development, cell proliferation, and apoptosis. By using genetic and biochemical approaches, the present study shows that E7 binds to E2F1in vivo and in vitro and that both proteins co-localize in the nucleus. Importantly, the binding of the high risk group HPV E7 to E2F1 is tighter than the binding of the low risk group HPV E7 to E2F1.
Several DNA tumour viruses target E2F proteins. These include Adenovirus, Epstein-Barr Virus (EBV), Simian Virus 40 (SV40), Hepatitis B virus (HBV), and Human Cytomegalovirus (HCMV):

Summary

The protein encoded by this gene is a member of the E2F family of transcription factors. The E2F family plays a crucial role in the control of cell cycle and action of tumor suppressor proteins and is also a target of the transforming proteins of small DNA tumor viruses. The E2F proteins contain several evolutionally conserved domains found in most members of the family. These domains include a DNA binding domain, a dimerization domain which determines interaction with the differentiation regulated transcription factor proteins (DP), a transactivation domain enriched in acidic amino acids, and a tumor suppressor protein association domain which is embedded within the transactivation domain. This protein and another 2 members, E2F2 and E2F3, have an additional cyclin binding domain. This protein binds preferentially to retinoblastoma protein pRB in a cell-cycle dependent manner. It can mediate both cell proliferation and p53-dependent/independent apoptosis. [provided by RefSeq, Jul 2008]

Expression

Broad expression in bone marrow (RPKM 12.7), testis (RPKM 5.6) and 17 other tissues"

From: “E2F1 E2F transcription factor 1 [ Homo sapiens (human) ]”

2.2 Osteoporosis

I was simply curious to see what signalling pathways there may be, if any, to link HPV and/or a vaccine to the anonymous case report of osteoporosis in a teenage boy. I quickly ruled out premature ovarian insufficiency…

Aside from the sex of the patient, POI-associated osteoporosis usually develops over several years. It is probably a secondary effect, more akin to bone loss associated with premature menopause. Whereas in the case report, we may have a more acute disease occurrence, but we don’t know his vaccination history or timescales.

I expected there to be an association, though, as many vaccines promote systemic inflammation as part of the immune response. As we shall see later, cytokine levels may remain elevated for several weeks or months, and again after each booster dose or infection-associated antigen exposure.

Pro-inflammatory cytokines have a well-researched effect on the bones of the human skeleton, and can disrupt a delicate balance. They tend to promote bone-resorbing osteoclasts over bone-forming osteoblasts. This is a necessary part of maintaining a healthy bone structure, but taken to excess may lead to weakness and impaired healing ability.

I’ve written about this before, with respect to SARS-CoV-2 and engineered spike glycoprotein.

Illustrations of an osteoblast and osteoclast in a femur (thigh bone).
“Osteoblasts and osteoclasts work together to form new bone cells and break down old or damaged bone tissue.” Source: https://my.clevelandclinic.org/health/body/24871-osteoblasts-and-osteoclasts
A way to remember which does which:

“Think clasts for cleaners and blasts for builders”.

What do osteoblasts do?

Osteoblasts are like construction crews that build new bone cells. You might see them called osteogenic cells. They strengthen your existing bones and help form new bone tissue.

Osteoblasts have three main functions:

Growing new bones (bone formation).
Reshaping bones to help them change as you age (remodeling).
Healing damaged or broken bones.
Osteoblasts are triggered by chemical reactions or hormones when a bone grows or changes. They create and release (secrete) a mix of proteins called bone matrix. Bone matrix is made of proteins like collagen mixed with calcium, phosphate and other minerals.

After they’re activated, osteoblasts move into place and deposit bone matrix in spaces on a bone that needs to grow or be strengthened or repaired. After it’s in place, the bone matrix solidifies and hardens into new, healthy bone. Picture a worker pouring concrete. They might create a whole new sidewalk. But they can also use that same concrete to patch cracks or broken chunks in an existing path. In this example, osteoblasts are the worker, and bone matrix minerals are the concrete they use to create new bone.

Once the osteoblasts have completed their job of laying down new bone tissue, they can then become part of the bone by transforming (differentiating) into osteocytes, or they die (if they’re no longer needed).

Osteocytes act like a security system inside your bones. They’re the most common type of cell in your bones. They monitor changes in pressure and stress that affect your bones. They respond to everything from normal movement and the force of you using your body to more intense changes like injuries. They can send signals to the osteoclasts and osteoblasts to repair damaged bone tissue. For example, if a bone is cracked, damaged or broken, osteocytes trigger a reaction that attracts osteoclasts to dissolve the area around the break (to resorb damaged bone tissue) and osteoblasts to lay down new bone tissue, so it can begin to heal.

What do osteoclasts do?

Osteoclasts dissolve and break down old or damaged bone cells. They make space for osteoblasts to create new bone tissue in areas that are growing or need repair.

If osteoblasts are builders, osteoclasts are your bones’ demolition crew. Think clasts for cleaners and blasts for builders. Osteoclasts release enzymes that break down old bone. They trigger chemical reactions on the surface of old bone tissue that dissolves it and creates space for newer, stronger tissue to form in its place.

Osteoclasts dissolve bone tissue, but it’s not as violent or aggressive as acid eating a hole in metal in a cartoon. The process of breaking down areas of old tissue is tightly regulated or controlled and specific. Osteoclasts only target specific areas that have been tagged by osteocytes.

The enzyme osteoclasts release breaks down hardened bone matrix and reabsorbs it into your body. This leaves microscopic pits and divots on the surface of your bone. Once the targeted tissue in those places is dissolved, osteoblasts move in and deposit new bone in the same spot.

Anatomy

What do osteoblasts and osteoclasts look like?

Osteoblasts and osteoclasts are tiny cells found along the bone lining and in the bone itself.

Osteoblasts are shaped like cubes — they’re slightly box-shaped.

Osteoclasts are bigger than osteoblasts. They’re shaped like rounded domes.

More: https://my.clevelandclinic.org/health/body/24871-osteoblasts-and-osteoclasts

Our health represents the sum total of multiple factors. These include our familial genetic lottery, lifestyle and epigenetics, infection history, and the effects of a cocktail of different allopathic meds and vaccine programs.

Inflammation goes hand-in-hand with a robust immune response in response to vaccination.

If multiple vaccines and drugs are being administered, e.g. for HPV, SARS-CoV-2, influenza, shingles, corticosteroids, etc., then the risk of systemic immune-inflammation could be disproportionately increased further than just through HPV vaccines alone. Very few to no clinical trials will have been conducted to look at this type of interaction.

Unfortunately, even a 2% reduction in bone mineral density can lead to a significantly increased risk of fracture.

Purpose

This study aims to investigate the associations of the systemic immune-inflammation index (SII) with bone mineral density (BMD) and osteoporosis in adult females from a nationally representative sample.

… Considering osteoporosis as a risk factor for fracture, it is possible that SII could be a risk factor for fracture. Our results showed that the reduction of BMD could reach 2% with a doubling of SII change. A previous study using a meta-regression of published trials found a 2% improvement in femoral neck BMD was associated with a 28% reduction in vertebral fracture, a 15% reduction in hip fracture, and a 11% reduction in nonvertebral fracture (30). Thus, these about 2% reductions of BMD with a doubling of SII could be large enough to affect fracture risks.

Figure 2
Figure 2. Efficacy of SII in discriminating osteoporosis in postmenopausal women. Receiver operating characteristic (ROC) curves of SII in discriminating osteoporosis regarding the total femur (A), femur neck (B), trochanter (C), and intertrochanter (D) as well as overall osteoporosis (E) are presented.
From: “Systemic immune-inflammation index is associated with decreased bone mass density and osteoporosis in postmenopausal women but not in premenopausal women“ (2023)

https://pmc.ncbi.nlm.nih.gov/articles/PMC9986387/

To investigate the pathways, as with any complex task, it’s useful to break the process down into logical steps.

Research step 1:

HPV is associated with a significantly increased risk of osteoporosis, according to at least two studies:

“Human Papillomavirus Infections and Increased Risk of Incident Osteoporosis: A Nationwide Population-Based Cohort Study” is from 2023, by Sheng-Kai Ma et al⁴:

… The cumulative incidence of osteoporosis in patients with HPV was significantly higher than that in non-HPV controls (log-rank test p-value = 0.01) (Figure 1). The Cox proportional hazards regression models revealed that patients with HPV infections presented with significantly greater risk of osteoporosis (aHR = 1.32, 95% CI = 1.06–1.65) (Table 2). Consistent with previous studies [1,35,36], the risk of osteoporosis was lower in men (aHR = 0.23; 95% CI = 0.18–0.3), and in populations of high socioeconomic status [37] (aHR = 0.30; 95% CI = 0.14–0.64); while the risk of osteoporosis was higher in frequent out-patient department (OPD) visitors (aHR = 1.01; 95% CI = 1.01–1.01) and in patients with comorbidities including COPD (aHR = 1.35; 95% CI = 1.08–1.68), vitamin D deficiency (aHR = 18.3; 95% CI = 2.56–131.09), long term glucocorticoid use (aHR = 2.05; 95% CI = 1.44–2.92), and TCAs/SSRIs use (aHR = 1.60; 95% CI = 1.05–2.43). The risk of osteoporosis was also higher in the older age groups [38], in which patients aged between 60–70 (aHR = 4.29; 95% CI = 3.10–5.93), aged between 70–80 (aHR = 7.32; 95% CI = 5.23–10.26) and aged beyond 80 (aHR = 9.63; 95% CI = 6.22–14.88) were associated with a significantly high risk of osteoporosis (Table 2< HPV疫苗相关病理：骨质疏松症和癌症途径 - 第10节第10节APP阅读时间阅读：短篇小说 - Novelette - Novella - 小说 - 博士 - 博士 - 特朗普的关税清单 - 战争与和平 - 美国税收 Mark Deeks在linkedin：#chatgpt #content #authenticity #thatpianguy | 27条评论手写。 没有幻觉或宣传。 高地图集山豪华旅行 - 2025年度量身定制的假期| Jacada Travel High Atlas Mountains，摩洛哥中部，北非内容1.0引言1.1神经代理攻击？ 1.2人乳头瘤病毒（HPV）2.0讨论2.1病毒致癌机制2.2骨质疏松症HPV疫苗L1蛋白与免疫细胞的细胞因子对HPV疫苗和癌症途径的结合3.0 在人乳头瘤病毒疫苗接种后，日本女孩们已经注意到慢性肢体疼痛的一种相对较高的慢性肢体疼痛，经常复杂化。 第一剂疫苗的平均潜伏期为5.47±5.00个月。 频繁的表现因素包括头痛，一般疲劳，脚的寒冷，肢体疼痛和弱点。 用肢体症状的女孩的皮肤温度在手指略低，脚趾中度较低。 数字体积素表揭示了波浪的峰值，特别是在脚趾中。 受影响女孩的肢体症状与复杂的区域疼痛综合征的诊断标准兼容。 Schellong试验确定了大量的患有原位低血压的患者和少数姿势外畸形心动过速综合征。 皮内神经的电子微观检查在检查的三个女孩中的两种女孩中，在未键合纤维中表现出异常病理学。 本研究中观察到的症状可以通过异常的外周交感神经反应来解释。 患者中最常见的先前诊断是心理疾病。 最近，接种后女孩在接种后的女孩中的认知功能障碍的延迟表现引起了注意力。 症状包括记忆丢失和读取教科书和/或计算的困难。 来自：“HPV疫苗接种中的神经系统并发症”（2015）Lewis Carroll Quote：“这一切都在你的头上，爱丽丝。” 1.2人乳头瘤病毒（HPV）HPV属于乳头瘤病毒系列DNA病毒。 它通常感染身体的皮肤和粘膜。 有一百多种HPV。 虽然大多数这些感染无害地清除，但某些类型的生殖器HPV可能导致肿瘤转化，导致子宫颈癌症。 HPV也与肛门，阴茎，阴道，外阴和喉咙背部的癌症有关（Oropharyngeal癌症）¹。 未定义的“HPV型病毒衣壳蛋白的低温电子显微镜结构。 从PDB呈现：5Keq [112]“。 由Opabinia Regalis - 自己的工作，CC By-SA 4.0，HTTPS://Commons.Wikimedia.org/w/Index.php?curid=80562689来自Wiki：“性传播的HPV是 低风险HPV导致生殖器上或周围的疣。 6型和11种导致90％的生殖器疣和复发性呼吸乳头状病，导致空气通道中的良性肿瘤。 高风险的HPVs导致癌症，由大约十二种确定类型组成。[11] 类型16和18的类型负责导致大多数HPV导致的癌症。 这些高风险HPV导致世界上5％的癌症。 在美国，高风险的HPVs导致女性癌症患者的3％和男性2％。[92] 持久性生殖器HPV感染的危险因素增加了发展癌症的风险，包括第一性交，多个合作伙伴，吸烟和免疫抑制的早期时代。[1]“这种词条将简要讨论HPV诱导的肿瘤转化和 免疫引发有助于介导观察到的长期效果。 我被提示调查公民记者后的病理学，欠款分享了这一匿名职位：这项工作并不排除其他疫苗诱导的病理学的贡献，例如过早的卵巢不足（POI）²，这一直受到各种影响 这些包括骨质疏松症的索赔，心脏病和盆。 证据的负担很高，而不是你有利于你。 （仅供参考，不是认可）：我们的律师正在帮助想要在美国举行Gardasil HVP疫苗诉讼的受害者。 我们的律师事务所特别关注卵巢衰竭病例，导致在过去几年中养殖Gardasil的妇女的不孕症。 Gardasil是一种旨在预防人乳头瘤病毒（HPV）的疫苗，其有时会导致女性的宫颈癌。 Gardasil是由武装的制药公司Merck＆Co.Merck于2006年获得FDA批准的基于欺骗性的研究和临床试验，以歪曲疫苗的疗效，同时隐瞒其安全风险和副作用。 然后，默克推出了一个积极的和高度误导的营销活动，包括数百万父母接种他们的前青少年女儿与Gardasil接种。 提交Gardasil诉讼不是反vax声明。 Gardasil疫苗诉讼是一个声明，我们所有人都假定的这种特定疫苗可能不是安全。 Gardasil Settlement预测不同类型的伤害Gardasil Class诉讼诉讼更新于4月25日2025年4月25日 - 在Gardasil疫苗MDL在贝尔法官之后向第四巡回疫苗提出了对第四次电路的呼吁放置原告。 原告开放申诉介绍于2025年5月27日.2025年3月12日 - 北卡罗来纳州西区MDL法官的艰难裁决已裁定默克，并就隐含抢先的理由授予摘要判决。 该决定有效地阻止了原告所带来的失败，据称，默克的原告应该包括关于姿势直向性心动过子综合征（盆栽）和Gardasil标签上的原发性卵巢不足（POI）的警告。 还有其他索赔，但现实是这是未能警告案例。 所以它是MDL中的粉碎。 法院发现，在联邦法律下，如果没有FDA批准，默克无法独立增加这些警告。 由于FDA从未要求此类警告 - 并且一直被拒绝涉及Gardasil导致盆栽或POI-法院确定国家法律失败的索赔与联邦监管冲突，因此抢先抢占。 裁决是联邦诉讼中默克的主要胜利，因为它消除了原告的中央法律索赔之一。 该决定不适用于州法院案件。 因此，虽然这一裁决很重要，但它并没有完全结束Gardasil诉讼。 该决定仅适用于联邦法院MDL综合的案件。 州法院诉讼仍未受到影响，原告仍然可以根据国家法律追求索赔，特别是在涉嫌对未经警告索赔的司法管辖区，或者在欺诈，疏忽或设计缺陷的诸如欺诈，疏忽或设计缺陷的地方进行治疗。 国家和联邦诉讼之间的对比已经显而易见。 洛杉矶的一个国家法院审判，一个涉嫌甘露西尼的妇女带来了一种心脏病的心脏条件，最近由于潜在的陪审团偏见而被推迟。 延迟源于罗伯特F.肯尼迪JR的确认。作为美国卫生和人类服务部长。 肯尼迪是一个长期批评疫苗的批评，据律师事务所处理Gardasil诉讼，并在将他的儿子转移到他的儿子之前，从一些这些诉讼中被设定为财务受益。 他的高度公布的确认过程导致陪审员可能受到他疫苗相关的倡导的影响。 因此，尽管这种联邦抢救裁决，但更广泛的Gardasil斗争仍未结束。 国家法院将继续听取案件，以及默克披露的法律战斗是否充分披露Gardasil的风险将在这些司法管辖区中发挥作用。 默克在MDL的胜利意味着联邦原告现在可以专注于其他索赔，例如欺诈或设计缺陷，而州法院诉讼仍然活跃。 2025年3月8日 - 为什么Gardasil不在疫苗宫廷里，Gardasil被VICP覆盖，这意味着个人在Gardasil造成伤害必须在疫苗法院提出申请，然后才能起诉制造商。 然而，Gardasil未列出疫苗损伤表，该疫苗损伤表概述了所假定在定义的时间范围内由特定疫苗引起的特定损伤。 因为加拿大人不在桌子上：根据联邦政府（也许肯尼迪为本）索赔人并没有得到索赔人的合法推控的利益，没有与之相关的推定伤害。 他们必须证明，使用医疗记录和经常专家证词，疫苗造成伤害。 没有桌子伤害的好处：证据负担更高。 索赔人必须表明疫苗“更有可能不是”造成伤害（证据优势）。 这通常需要保留昂贵的医学专家和组装详细的科学争论。 更多：https://www.lawsuit-information-center.com/gardasil-hpv-vaccine-lawsuit.html 2.0讨论2.1病毒致癌机制来自2002年由Hwang et “人乳头瘤病毒16E7与E2F1结合并以视网膜母细胞瘤蛋白无关的方式激活E2F1驱动的转录”³。 低风险的HPV类型对E2F1的强烈粘合E7蛋白，肿瘤抑制剂。 强的结合有助于更高风险的HPV来阻止E2F1限制癌细胞分裂：人乳头瘤病毒（HPV）E7癌蛋白可以永生化原发性细胞并诱导肿瘤形成。 E7的这些性质取决于其抑制视网膜母细胞瘤蛋白（PRB）活性的能力，这反过来影响E2F功能。 E2F蛋白质控制参与分化，发育，细胞增殖和细胞凋亡的基因的表达。 通过使用遗传和生化方法，本研究表明，E7与E2F1IN体内和体外结合，并且两种蛋白质在细胞核中共定位。 重要的是，高风险组HPV E7至E2F1的结合比低风险组HPV E7至E2F1的结合更严重。 几种DNA肿瘤病毒靶向E2F蛋白。 这些包括腺病毒，epstein-barr病毒（EBV），Simian病毒40（SV40），乙型肝炎病毒（HBV）和人巨细胞病毒（HCMV）：发明内容该基因编码的蛋白质 E2F家族在控制细胞周期和肿瘤抑制蛋白的作用中起着至关重要的作用，也是小DNA肿瘤病毒的转化蛋白的靶标。 E2F蛋白质含有在大多数家庭成员中发现的几个进化保守域。 这些结构域包括DNA结合结构域，其确定与分化调节的转录因子蛋白（DP）相互作用的二聚化结构域，富含酸性氨基酸的反式激活结构域，以及嵌入其中的肿瘤抑制蛋白质结区间 该蛋白质和另外2个成员，E2F2和E2F3具有另外的细胞周期蛋白结合结构域。 该蛋白优先以细胞周期依赖性方式对视网膜母细胞瘤蛋白PRB结合。 它可以介导细胞增殖和依赖于P53依赖性/独立的凋亡。 [由Refseq，Jul 2008]提供的骨髓（RPKM 12.7），睾丸（RPKM 5.6）和17种其他组织中的表达宽表达：“E2F1 E2F转录因子1 [Homo Sapiens（人）]” 促炎细胞因子对人体骨骼的骨骼具有良好研究的影响，并且可以破坏微妙的平衡。 它们倾向于促进在骨形成成骨细胞上的骨再吸收骨质蛋白。 这是保持健康骨骼结构的必要部分，但过度可能导致愈合能力有弱点和受损。 我以前写过这一点，关于SARS-COV-2和工程尖刺糖蛋白。 成骨细胞和骨酸骨骨的例证在股骨（大腿骨）。 “成骨细胞和骨壳组合在一起形成新的骨细胞并分解旧或受损的骨组织。” 资料来源：https://my.clevelandclinic.org/health/body / 24871-oxteoblasts-and-osteoclasts一种方法要记住哪些方法：“思考垃圾箱，为建筑商的清洁剂和爆炸”。 成骨细胞做了什么？ 成骨细胞就像建造新骨细胞的建筑船员。 你可能会看到它们称为骨质细胞。 他们加强了现有的骨骼并帮助形成新的骨组织。 成骨细胞有三个主要功能：生长新骨骼（骨形成）。 重塑骨骼以帮助它们随着年龄的增长而改变（重塑）。 愈合损坏或破碎的骨头。 当骨长或变化时，通过化学反应或激素触发成骨细胞。 他们创造和释放（分泌）一种称为骨基质的蛋白质。 骨基质由胶原蛋白与钙，磷酸盐和其他矿物混合的蛋白质制成。 在它们被激活后，成骨细胞在需要生长或加强或修复的骨骼上的空间中进入放置和沉积骨基质。 在它到位之后，骨基质凝固并硬化为新的健康骨骼。 图片工人倾吐混凝土。 他们可能会创造一个全新的人行道。 但它们还可以使用同样的混凝土来修补现有路径中的裂缝或破碎的块。 在该实施例中，成骨细胞是工人，骨基质矿物质是它们用于产生新骨的混凝土。 一旦成骨细胞完成了铺设新骨组织的作业，就可以通过将（将）转化为骨细胞来成为骨的一部分，或者它们死亡（如果它们不再需要）。 骨细胞就像骨骼内的安全系统一样。 它们是骨骼中最常见的细胞类型。 它们监测影响您骨骼的压力和压力的变化。 他们从正常运动和你身体的力量响应了从正常运动和力量更加强烈的变化。 它们可以向破骨细胞和成骨细胞发送信号以修复受损骨组织。 例如，如果骨骼被破裂，损坏或破裂，骨细胞引发了吸引骨细胞以溶解突破周围的区域的反应（以反销受损的骨组织）和成骨细胞，所以它 骨核糖蛋白是什么？ 骨核苷酸溶解并分解旧骨细胞或受损骨细胞。 它们为成骨细胞制造空间，以在生长或需要修复的区域中产生新的骨组织。 如果成骨是建筑商的，骨质骨液是你的骨头拆迁机组人员。 思考Clasts为制造商的清洁剂和爆炸。 破骨细胞释放酶，分解旧骨骼。 它们触发在溶解它的旧骨组织表面上的化学反应并为新的较低的组织产生空间，以形成其位置。 骨酸骨溶胶溶解骨组织，但它并不像酸在卡通中吃金属洞一样暴力或侵略性。 断开旧组织区域的过程紧密调节或控制和具体。 骨核苷酸仅靶向由骨细胞标记的特定区域。 酶骨壳释放释放出硬化的骨基质并将其重新吸入您的身体。 这使得微观坑和骨骼表面上的凹坑。 一旦这些地方的靶向组织溶解，成骨细胞在同一点进入并沉积新骨。 解剖骨细胞和破骨细胞的样子是什么样的？ 成骨细胞和疏口细胞是沿着骨衬里和骨骼本身的微小细胞。 成骨状成形为立方体 - 它们略微盒状。 骨核糖籽大于成骨细胞。 它们形状像圆角。 更多：https://my.clevelandclinic.org/health/body / 24871-osteoblasts-and-osteoclasts我们的健康代表了多种因素的总和。 这些包括我们的家庭遗传彩票，生活方式和表观遗传学，感染历史，以及不同来自疗法药物和疫苗计划的鸡尾酒的影响。 炎症伴随着抗疫苗接种的鲁棒免疫反应携手共进。 如果施用多种疫苗和药物，则为例如疫苗和药物。 对于HPV，SARS-COV-2，流感，带状疱疹，皮质类固醇等，那么系统性免疫炎症的风险可能比单独通过HPV疫苗更加不成比例地增加。 很少有没有临床试验，以看待这种类型的互动。 遗憾的是，骨矿物密度的2％降低甚至可能导致骨折的显着增加。 目的本研究旨在调查来自全国代表性样本的全身免疫炎症指数（SII）与骨密度（BMD）和骨质疏松症的关联。 ...考虑骨质疏松症作为骨折的危险因素，SII可能是骨折的危险因素。 我们的研究结果表明，BMD的减少可以达到2％，随着SII变化加倍。 使用出版试验的荟萃回归的先前研究发现，股骨颈BMD的2％改善与椎骨骨折的28％有关，髋部骨折降低15％，髋部骨折减少11％（30 因此，这些约2％的BMD减少了与SII加倍的BMD可能足够大以影响裂缝风险。 图2图2. SII在绝经后妇女歧视骨质疏松症中的疗效。 SII的接收器操作特征（ROC）曲线在鉴别关于总股骨（A），股骨颈（B），Troochantor（C）和血管转子（D）以及总骨质疏松症的骨质疏松症（ 来自：“全身免疫炎症指数与绝经后妇女的骨质密度和骨质疏松症有关，但未在前进女性中有关，但在前一妇女（2023）https://pmc.ncbi.nlm/ 研究步骤1：根据至少两项研究，HPV与骨质疏松症的风险显着增加：“人乳头瘤病毒感染和发生骨质疏松症的风险增加：全国群体的队列研究”是从202年开始 Cox比例危害回归模型显示HPV感染的患者呈现出骨质疏松症的风险明显更大（AHR = 1.32,95％CI = 1.06-1.65）（表2）。 与先前的研究一致[1,35,36]，男性骨质疏松症的风险较低（AHR = 0.23; 95％CI = 0.18-0.3），以及高社会经济地位的群体[37]（AHR = 0.30 虽然频繁的门诊部（OPD）访客（AHR = 1.01; 95％CI = 1.01-1.01）和包括COPD（AHR = 1.35; 95％）的患者患者骨疏松症的风险较高 年龄较大的群体骨质疏松症的风险也在更高[38]，其中患者在60-70（AHR = 4.29; 95％CI = 3.10-5.93）之间，年龄在70-80（AHR = 7.32; 95之间