#hyperproliferative

[jcmicr]

A rare case of bilateral plantar fibromatosis (Ledderhose’s disease): A case report by Amrutha Viswanath in Journal of Clinical and Medical Images, Case Reports  

Abstract

Ledderhose’s disease, also known as plantar fibromatosis is a rare, benign hyperproliferative disorder affecting plantar fascia with unknown etiology. Clinical presentation of the disease varies according to the stage of the disease and individual characteristics. Diagnosis of the disease is usually based on clinical findings. Histopathological examination, Ultrasound or MRI can be used to rule out other conditions and for confirmation of the disease. Plantar fibromatosis can mimic the features of plantar fasciitis especially in early stages of the disease, hence it should be considered as a differential diagnosis in patients with pain and nodules in plantar aspect of foot. In this case report, we present a case of 24-year-old male with bilateral plantar fibromatosis, which was managed by surgical excision of the nodules due to unresponsive conservative management.

Keywords: Plantar fibromatosis; ledderhose’s disease; heel pain; nodular swelling; plantar fasciitis.

Introduction

Plantar fibromatosis or Ledderhose disease, is a rare benign pathology of the plantar aponeurosis, first described by Dr. George Ledderhose. It is characterised by disordered fibrous tissue proliferation and the subsequent formation of lump or nodules over the plantar aspect of the foot. The Office of Rare Diseases of the National Institutes of Health listed it as a rare disease with frequency about 1–1.75/100,000 [1]. Although etiology of plantar fibromatosis is unknown, it is associated with Dupuytren’s disease (palmar fibromatosis), Peyronie’s disease (penile fibromatosis) [2]. Increased risk of its occurrence is associated with alcoholism, chronic liver disease, diabetes mellitus, long term anticonvulsive treatment for epilepsy and genetic factors [3]. Males are more commonly affected than females. 25% of cases with plantar fibromatosis present with bilateral disease [4]. Diagnosis of Ledderhose’s disease is usually established clinically. Initially the nodule is asymptomatic and it becomes symptomatic as it enlarges in size. Direct pressure on the nodule while walking barefoot, standing for long periods of time and use of restrictive shoes may exacerbate pain and walking disability. Over time, multiple nodules may develop and can cause exacerbation of symptoms, contractures and deformities [5]. Given the benign nature, initial phase of the disease can be managed conservatively and if symptoms persist, definitive management of surgical excision of nodule gives complete relief of symptoms. The nodular swellings affecting the plantar fascia is of greater significance in population with poor socioeconomic status as people prefer to walk barefoot in developing countries.

The similarities of plantar fibromatosis to Dupuytren's disease affecting palmar fascia support the theory that, two conditions are different expressions of the same disorder [6]. Even though much has been discussed about Dupuytren's contracture in the literature; only very few literatures are available regarding plantar fibromatosis. In this case report, we present a case of 24-year-old male with bilateral plantar fibromatosis and aims to discuss the clinical presentation and various management options in plantar fibromatosis.

Case Report

A 24-year-old male presented to our department with dull aching type of pain over the plantar aspect of both feet of 1-year duration. Pain prevented the patient from weight-bearing for long time and walking for small distances. There was no significant familial history of the disease or history of any associated trauma. No associated medical history in the patient. Patient gives history of treatment in another hospital as bilateral plantar fasciitis. Conservative management was given there in the form of analgesics, anti-inflammatory drugs, advice to use footwear with soft insole and gives a history of 3 steroid injections administered 4-6 weeks apart. With persistence of symptoms patient came to our department. On physical examination small, well circumscribed, palpable, firm, nodular, single swelling was present over the medial plantar aspect of his both feet. The swellings measured about 2 x 1.5 cm on the right foot and 1 x 1 cm on the left foot. The skin over the swellings appeared normal and there were no neurovascular deficits or deformities. Ankle joint and foot range of movements were within normal range. On further examination, we found a similar swelling of size 0.5 x 0.5 cm on the palmar aspect of right hand with no restriction of movements and clinical signs. FNAC report showed mild to moderately cellular oval to plumb spindle shaped fibroblastic cells with elongated nuclei arranged in clusters and dispersed pattern associated with myxoid matrix. Cytology findings were suggestive of benign fibroblastic lesion. A provisional diagnosis of bilateral plantar fibromatosis was made, based on clinical and cytological findings. Since conservative management was tried earlier and there was persistence of symptoms and limitation in function surgical excision of the nodules was planned. Surgery was performed under spinal anesthesia. Nodules on both sides were palpated and skin over it was marked for surgical incision. The dissection of skin and soft tissue exposed the nodules on both sides, which were greyish white in colour, firm in consistency and attached to plantar fascia (Figure 3).

Figure 1: Nodular swelling on right foot (dot circle).

Figure 2: Dot circle indicating the nodular swelling on right palm.

Figure 3: Exposed nodule ( Right foot ) intraoperative image.

Figure 4: Excised nodule from right foot (greyish white, measuring 1x0.8x0.2 cm).

Figure 5: Excised nodule from left foot (greyish white to greyish brown, measuring 1.7x1.5x0.4 cm).

Excision of the nodules were done in both feet and primary wound closure was done. The patient was advised for non-weight bearing for 2 weeks and use of soft insole footwear thereafter for 2 weeks. Postoperative period was uneventful and sutures were removed after 2 weeks of surgery.

Figure 6: Postoperative wound before suture removal.

The histopathological examination of the excised nodules revealed spindle-shaped cells with abundant collagen in a fibrous stroma background and features were consistent with the diagnosis of bilateral plantar fibromatosis. On follow up of 6 months, patient reported complete relief of symptoms and improvement in function.

Figure 7: Photomicrograph of HPE slide showing nodular lesion composed of spindle shaped cells in a fibrous stroma background. (H&E staining, x40).

Figure 8: Photomicrograph of HPE slide showing spindle shaped cells with abundant collagen in fibrous stroma(H & E staining , x100).

Discussion

Ledderhose’s disease (Plantar fibromatosis) is a fibrous hyperproliferative pathology affecting the plantar fascia characterised by formation of nodules [7, 8]. The diagnosis of Ledderhose’s disease is usually established clinically and rarely require further investigations for confirmation [9]. Histopathological analysis and diagnostic imaging helps to differentiate between other lesions that can present with similar symptoms such as plantar fasciitis ( The most common disorder of plantar fascia), lipoma , ganglion cyst, leiomyoma, epithelioid sarcoma, rhabdomyosarcoma and liposarcoma [10, 11]. According to the clinical and pathological studies, plantar fibromatosis can be classified into three stages. The first (proliferative) stage of the disease is characterised by cellular proliferation and increased fibroblastic activity. The second stage of the disease which is the active phase is characterised by formation of nodules. It is followed by the third (residual) stage where collagen maturation and tissue contractures occur [11, 12]. Therefore the normal plantar fascia is replaced progressively by abnormal collagen fibres and can present at any stage of the disease with pain, nodule, walking difficulty, contractures or deformities of toes and the treatment is planned accordingly.

Patients presenting in the early stage of the disease with no or mild pain can be conservatively managed with padded shoes with soft insoles or custom offloading to redistribute the weight from the nodules, analgesics, anti-inflammatory drugs and intralesional steroid injections[10,13]. If left untreated, nodules may gradually increase in size and number which in rare cases may result in deformities of the toes due to contractures in later stages. In cases with persistence of symptoms after conservative management, lesions which are progressive, severe limitation of function and in advanced stages of the disease surgical management is considered as the last resort of treatment [14, 15].

The nodular swellings affecting the plantar fascia is of greater significance in developing countries with poor socioeconomic status as people prefer to walk barefoot. For the same reason, early surgical management is indicated for symptomatic cases in the developing countries.

Conclusion

The diagnosis of Ledderhose’s disease can be done clinically alone. Diagnostic imaging such as Ultrasound or MRI and histopathological examination may be used, to exclude other conditions and to rule out malignancies [16]. The treatment of the disorder is planned accordingly. Even though plantar fasciitis is the commonest disorder affecting plantar fascia, plantar fibromatosis should be considered as a differential diagnosis in patients presenting with pain and nodules in plantar aspect of foot as it can mimic the features of plantar fasciitis. The recommended treatment approach is to start with conservative management in early stages of the disease and perform surgical excision in unresponsive cases and advanced stages. But the best treatment plan is to establish a personalised approach depending on the individual characteristics, type of symptoms, stage of the disease and recurrence.

Authors Disclosures:

Funding / Grants: Nil.

In this study, there was no competing interests or financial benefits to the authors.

Details of any previous presentation of the research, manuscript, or abstract in any form: Not presented anywhere.

Acknowledgement:

Authors declare no conflict of interest.

In this case report, there is no financial benefits to the authors.

For more details : https://jcmimagescasereports.org/author-guidelines/ 

[alfalfaaarya]

17 April 2024//Wednesday

Day 1 of Productivity streak

Got done with 5/6 things on my to study list .

Completed

Micro : Bacteria anatomy and Physiology

Pathology: Acute Inflammation

RBC , Reticulocyte, Indices and

Hyperproliferative anemias

Also completed patho clinical journal write up and a bit of general patho journal write up .

Felt good to be productive after a long time !

Adios

🙏

[kittenkes]

So I guess it's pretty standard practice to inject factory farm animals with pregnant horse blood so that they become instantly fertile again after birth.

Oh, and it's pretty normal that we inject them again to induce labor so that it fits within our industrial work day. Plus, it keeps workers productive at all times because what's the alternative?

Oh and it's perfectly normal that we genetically create hyperprolific animals that carry twice as many babies so the factory can save money, even if the babies come out weaker and mortality rates grow.

And it's normal to sacrifice some of these weak runts by putting them in igloo coolers that fill up with CO2, especially if there's a chance that a fraction of the runts will grow up and be sold as meat and make the company more money.

[self-loving-vampire]

🔥 hyperprolific early-mid internet creators eg kc green, neil c, etc

I am not very familiar with them and so I am indifferent.

[byneddiedingo]

Yoshiko Kuga and Teiji Takahashi in Thus Another Day (Keisuke Kinoshita, 1959) Cast: Yoshiko Kuga, Teiji Takahashi, Takahiro Tamura, Kazuya Kosaka, Kanzaburo Nakamura, Rentaro Mikuni. Screenplay: Keisuke Kinoshita. Cinematography: Hiroshi Kusuda. Production design: Chiyoo Umeda. Film editing: Yoshi Sugihara. Music: Chuji Kinoshita.  The hyperprolific Keisuke Kinoshita released two other films in 1959, and though Thus Another Day feels like it's crammed with ideas, they were given short shrift when it comes to working them out. It's a short feature, only 74 minutes, but it has enough plots and subplots for at least two movies. The central figures in the narrative are a married couple struggling to make ends meet. Shoichi (Teiji Takahashi) works in Tokyo while Yasuko (Yoshiko Kuga) stays home with their young son, Kazuo (Kanzaburo Nakamura). They have bought a house in the still semirural outskirts of the city, and Shoichi makes a mad dash for the bus every morning. Yasuko scrimps and saves, but receives scant praise for it from either Shoichi or their rather bratty child. Watching his mother do the wash by hand, Kazuo asks why they don't have a washing machine, and when she tells him they're saving up for it, he says he'd rather have a television set instead. Yasujiro Ozu treated the same kind of bullying juvenile materialism in a film made the same year, Good Morning, and Kazuo's blaming his father for not making more money is reminiscent of the children in an earlier Ozu film, I Was Born, But... (1932). Then Shoichi suggests that they rent out their house for the summer to a manager in his company who is looking for an escape from the city heat. It would not only help them pay the mortgage but would also curry favor with the higher-ups in the company. So Yasuko somewhat reluctantly agrees to take Kazuo and spend the summer with her family, who live in a resort area, while Shoichi bunks with a fellow employee in the city. At that point, the film begins to spin off into subplots and loses focus. Tension between Yasuko and Shoichi grows when he spends most of his occasional brief visits paying attention to his boss's wife, who is summering in the area. Yasuko befriends an older man who has a very young daughter to whom he is devoted, but when the little girl dies, he's sunk in a crippling, suicidal depression. The man's wife works at the resort, where some gangsters are hiding out and young thugs are bullying the locals, including a shy young man with a fine singing voice who is courting a local girl. Though all of these characters are interconnected in some way, Kinoshita never quite brings all of the relationships into focus, so when there's a murder disguised as an accident and an inevitable tragic denouement, these events don't have the impact they should. What does work in the film is Kinoshita's manipulation of atmosphere, from the sweltering city offices to the lush resort area, but this isn't enough to make the film more than a tantalizing sketch.

[medicaregate]

Anemia

Anemia is defined as a decrease in the number of red blood cells or hemoglobin in the blood. Anemia is a common nutritional deficiency disorder and a global public health problem that affects both developing and developed countries. It is a disease that affects up to one-third of the global population, but in many cases, it is mild and asymptomatic and does not require management. Anemia’s pathophysiology varies greatly depending on the underlying cause.

Anemia is caused by one of three different processes. Reduced red blood cells (RBCs) production, increased RBCs destruction, and blood loss the causes of anemia are also determined by whether it is hypoproliferative or hyperproliferative.

The signs and symptoms are weakness, lethargy, restless legs, shortness of breath, particularly on exertion, near-syncope, chest pain, and reduced tolerance to exercise. The majority of patients experience anemia-related symptoms when hemoglobin falls below 7.0 g/dL.

Common anemia types include iron-deficiency anemia, pernicious anemia, hemolytic anemia, sickle cell anemia, thalassemia, and aplastic anemia.  If anemia undiagnosed or untreated for a long time, it may result in multiorgan failure and even death. Chronic anemia most often affects the cardiovascular system. Anemia during pregnancy increases the risk of anemia in the baby as well as increased blood loss.

Family history, nutritional history, evaluation of vital signs, and laboratory measurements are all important in anemia diagnosis.  Anemia treatment depends mainly on treating the underlying cause of anemia, i.e., Anemia due to acute blood loss can be treated with IV fluids while Anemia due to nutritional deficiencies oral/IV iron, B12, and folate.  Focusing on foods high in iron, copper, zinc, folic acid, Vitamin B-12, and protein. The combination of iron and B vitamins is particularly beneficial in the treatment of anemia.

https://medicaregate.com/anemia/

[the-odd-job]

You wanna see the best motherfucking comment I’ve gotten on Harem AU? Don’t answer that, I’ll show it anyway.

HYPERPROLIFIC SADIST please someone write that on my gravestone. That’s how I want to be remembered.

[lupinepublishers]

Lupine Publishers | Micro-Environmental Systems and Endothelial Cells in Cooperative Tumorigenesis Account for Potential Malignant Transformation in Neurofibromatosis Type 1 Patients

Open Access Journal of Oncology and Medicine (OAJOM)

Lupine Publishers Open Access Journal of Oncology and Medicine (OAJOM)

Abstract

Overall tumorigenesis in neurofibromatosis type 1 patients constitutes a series of specific targeting events with a central role enacted by proliferation of fibroblasts and endothelial cells in overproduction of growth factors and cytokines such as transforming growth factor-beta and CXCL12 cytokine. The plexiform neurofibroma well-illustrates dimensions of such cooperative participation within operative fields of the initial Schwann cell proliferation leading in a significant number of patients to malignant transformation of the peripheral nerve sheath tumors. Inclusive directions in operative targeting of Schwann cells or astrocytes are staged performance in the transformation of hyperproliferative induction and constitute further evolutionarily defined incorporation of such systems as endothelial cells. Hyperproliferative cell subsets are initial and also consequential target formulation of potential malignant states as induced in malignant peripheral nerve sheath tumors.

Introduction

Neurofibromatosis type 1 (NF1) is a neurogenetic disorder and involves both heterozygous and homozygous absence/reduction of neurofibromin that acts normally as a tumor suppressor. There is a need to assess predisposing genetic factors and loss of heterozygosity causing emergence of aggressive neoplasms in patients with NF1 [1]. The two hit hypothesis helps account for the emergence of Schwann cell-based proliferations and for neurofibromas and plexiform neurofibromas. Gherkin may act on tumorigenesis of cutaneous neurofibromas via growth hormone secretagogue receptor [2]. It is important to consider the neurofibroma that is based on micro-environmental potentiation of tumor generation in patients that develop malignant nerve sheath tumors and astrocytomas in patients with NF1 +/- genotype; this occurs in a manner that involves growth factor overactivity and mast cell and endothelial overactivity within a milieu that dysfunctionally stimulates tumorigenesis. Reactive oxygen species overproduction lead to epithelial-mesenchymal transit in patients with neurofibromin deficiency and plays a crucial role in NF1 tumor growth [3]. RAS activation alone is not sufficient for malignant transformation of peripheral nerve sheath tumors; signal transduction may potentially help identify therapies for this neoplasm type [4].

Neurofibromin

The dynamics of neurofibromin as a cytoplasmic protein involve the regulation of K-Ras, and the PI3K/Akt pathways; absence of neurofibromin leads to overactivation of these pathways in various ways in inducing tumorigenesis in such lesions as optic tract pilocytic astrocytomas, brain stem astrocytomas and also other CNS astrocytomas in terms of progression of these lesions. The cell of origin determines the temporal course of neurofibromatosis-1 low-grade glioma formation [5]. The micro-environment of plexiform neurofibromas of peripheral nerves and of nerve plexi include a 10% risk of malignant change with subsequent aggressive clinical behavior in the affected patients. Over expression of cellular retinoid acid binding protein 2 is reported in several cancer types, including malignant peripheral nerve sheath tumors (MPNSTs) [6].

Related Tumor Predispositions

The neurofibromin insufficiency status in Schwann cells and fibroblasts allows for enhanced participation of immune system component cells such as microglia as evidenced in optic pathway low-grade astrocytomas. Telomere erosion is described in many tumor types and may potentially drive genomic instability and clonal progression in NF1-associated MPNSTs [7]. Tumor dimensions include proliferation of astrocytic cells in optic pathways, and of various subtypes of stromal cells such as fibroblasts and mast cells in the peripheral nervous system. It is significant to consider particularly the micro-environmental active participation in the genesis of the most common tumor type in Neurofibromatosis type 1 patient, that is the neurofibroma, which invokes proliferation of fibroblasts and endothelial cells. The congenital plexiform neurofibroma is in fact a hypervascular lesion that transgresses tissue margins and induces a significant risk for malignant transformation. NF1 loss is the primary driver of tumorigenesis in neurofibromatosis type 1-related plexiform neurofibroma [8]. It is further to such considerations that important cooperative intervention in malignant transformation of plexiform neurofibromas invokes multi-type cells in inducing proliferation of an integral Schwann cell-fibroblastic twin population in enhancing potential malignant transformation of the peripheral nerve sheath. A therapeutic window for neuroprotective intervention exists as detected by optical coherence tomography in mice with optic glioma, and particularly as an accurate biomarker of retinal ganglion cell apoptosis [9]. The heterozygous absence of one neurofibromin allele in mice results in plexiform neurofibromas and low-grade optic pathway astrocytomas. Mast cells appear to play a causal role in neurofibroma formation and also in microglia in optic pathway glioma evolution [10]. Such implications of the micro-enviromental factors includes a distinctive cooperative participation that carries implications for significant enhancement of cell proliferation and of such cytokines such as transforming growth factor and CXCL12 in formulating malignant transformation in such tumors. The methylemetetrahydrofolate reductase 1298 and 677 gene polymorphisms are related to optic glioma and hamartoma risk in NF1 patients through effects on DNA synthesis and methylation [11].

Convergent Targeting

The related tuberous sclerosis complex is analogous to neurofibromatosis type 1 as a neurogenetic disorder associated with increased risk for astrocytomas in the form of subependymal giant cell astrocytomas. A convergent targeting of systems of cell proliferation include in particular cyclic AMP and Ras in a manner that includes dimensions of micro-environmental conditioning. Mutations of the NF 1 gene are frequent in many cancer types in patients without NF1 and this is suggestive of a more general role for the NF1 gene in oncogenesis. In melanoma NF1 mutations potentially drive tumorigensis and promote drug resistance [12]. Inclusive dynamics allow for permissive tumorigenesis in a manner that includes the incorporation of malignant transformation within confines of a Schwann cell-fibroblast-endothelial cell system in the case of malignant peripheral nerve sheath tumors. Astrocytes and microglia are analogous counterparts in the induction of CNS astrocytomas. Such considerations are inclusive phenomena of multi-component induction of potential malignancy that recharacterizes conditioning of the micro-environment of proliferative states preceding tumorigenesis. Interaction between neoplastic Schwann cells and their surrounding neural microenvironment has important implications for early cellular events promoting tumorigenesis in neurofibroma development [13].

Performance Dynamics

Performance dynamics of tumors in neurofibromatosis type 1 may potentially modify the biologic significance of a two-hit hypothesis in a manner that implicates micro-environmental conditioning of the resultant cell hyperplasias and proliferations in such lesions as peripheral nerve sheath tumors and astrocytomas. NF1 provides unique vantage points to examine co-contributions of molecular, cellular, and tissue processes in tumor biology [14]. Such proposed dimensions invoke in particular an over-activation in production and action of growth factors that provoke selective malignant transformation of hyper-proliferative lesions composed of Schwann cells and astrocytes in the peripheral and central nervous systems respectively. Plasma soluble levels of transforming growth factor-beta and interleukin-6 are increased in NF1 patients and a shift towards an anti0inflammatory profile has been reported in cells expressing cytokines [15].

Hyperproliferation

The hyperproliferative states affecting Schwann cells and astrocytes invoke also fibroblast and microglial cell proliferations in a manner transforming tumorigenesis. Such facilitation to tumorigenesis invokes dimensions of transformation as well seen in plexiform neurofibromas that may undergo malignant transformation in a significant number of affected individuals. Such considerations are selective targeting of specific cell subpopulations in a manner that allows permissive transformation. Insertional mutagenesis identifies a STAT3/Arid1b/beta-catenin pathway that drives neurofibroma initiation in the context of Nf1 loss [16]. Mast cells and fibroblasts may potentially incorporate endothelial cells that may participate as central dysregulatory dimensions in plexiform neurofibroma tumorigenesis. The provocations for malignant transformation further cooperate in systems of derivative consequence as hypervascular lesions that subsequently lead to potential malignant cells in individual patients. Cross species comparative oncogenomic may identify driver mutations in mouse cancer models and allow validation in human tumors [17].

Concluding Remarks

Propositional implications in tumorigenesis include the multi-component participation of Schwann cells on the one hand and of fibroblasts, mast cells, endothelial cells and also of microglia in an inductive process that includes specific pathways of malignant transformation. Endothelial cell proliferation is related to substantial participation in modes related to key-events of increased proliferation of Schwann cells and astrocytes in initial stages of lesion infliction. Inclusive phenomena have thus become systems of consequence in affecting such specific cell proliferative states. Such events occur within the added dimensions of directed targeting of multiple-agent micro environmental modeling of the initial proliferation of the Schwann cells or astrocytes. A pivotal series of roles played by fibroblasts, endothelial cells, mast cells and of microglia and astrocytes appears a dynamic milieu within added consequences of malignant transformation of both Schwann cells and astrocytes that progress as cooperative systems of tumorigenesis.

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[labnotes19]

Some scientists publish more than 70 papers a year. Here’s how—and why—they do it

Science chats with statistician John Ioannidis about “hyperprolific” authors from Latest News from Science Magazine https://ift.tt/2N4klpj via IFTTT

[pigmentation21]

Psoriasis vedas cure

Psoriasis

What is Psoriasis?

Psoriasis is an immune system skin condition where the resistant framework assaults solid skin cells, however it likewise invigorates the development of skin cells. It isn't infectious, and it can occur in different pieces of the body.

Psoriasis is a constant provocative, hyperproliferative skin illness. It is portrayed by distinct, erythematous (widened skin veins) layered plaques with white surface scale (quick keratinocyte expansion) of infected skin frequently at destinations of minor injury especially influencing extensor surfaces, scalp, and nails, and generally follows a backsliding and transmitting course. As psoriasis is brought about by immunological aggravations, it isn't infectious. Psoriasis influences the skin as well as lead to joint inflammation (aggravation of the joints) in around 30% of patients.

There are 7 sorts of psoriasis with plaque psoriasis being the most widely recognized kind of psoriasis:

Plaque psoriasis

Nail psoriasis

Guttate psoriasis

Pustular psoriasis

Backwards psoriasis

Erythrodermic psoriasis

Psoriatic joint pain

The study of disease transmission of psoriasis

Geology: Globally 1-2% of the populace is influenced by psoriasis (125 million individuals in the UK/USA/Japan alone). It is less not unexpected in African, South American and Asian populaces; in any case, psoriasis influences roughly 1.5-3% of Caucasians.

Sex and age: Psoriasis influences both genders equally. It can introduce at whatever stage in life and in excess of half of patients present before the age of thirty years; despite the fact that it is seen once in a while before the age of five years. There is a bimodal dissemination old enough of beginning, with the beginning stage kind happening in pre-adulthood and early adulthood. This sort is generally extreme in power and patients frequently have a background marked by psoriasis in the family. The later-beginning kind presents between the ages of fifty and sixty, less serious and is emotional in power. Family ancestry is generally missing in this sort.

Pathophysiology of psoriasis

Both hereditary and ecological elements are significant. A kid who has one parent with psoriasis has a one of every four shot at fostering the illness. On the off chance that one indistinguishable (monozygotic) twin has psoriasis, there is a 70% possibility that the other will likewise be influenced; nonetheless, just a 20% possibility exists in the non-indistinguishable (dizygotic) twins. There is presently huge examination work showing that psoriasis is additionally connected with other significant comorbidities, for example, type 2 diabetes (expanded danger of 1.4 occasions), sadness, stoutness, cardiovascular sickness, and diminished personal satisfaction. Natural variables include:

Injury: Lesions can show up at destinations of skin injury, like scratches or careful injuries. This wonder is named the Köbner isomorphic marvel.

Disease: Throat contaminations frequently go before guttate psoriasis. Extreme psoriasis might be the underlying show of HIV disease.

Daylight: Psoriasis may happen or deteriorate after sun openness.

Medications: Many medications including antimalarials, β-blockers, lithium, and Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) can compound psoriasis. Bounce back; flare of psoriasis is regularly shaky and possibly pustular and may happen after the withdrawal of steroids.

Mental variables: Anxiety and stress may worsen psoriasis in inclined people.

Our consideration group will assist you with your psoriasis. We realize it tends to be difficult to live with psoriasis. With a very long time of face to face and advanced clinical experience treating psoriasis, we realize what works, and at costs that will not burn through every last cent. Try not to stop for a second to be assessed, so we can treat you. One of our online specialists can see you now.

Photographs

Psoriasis on the elbow of the patient. Psoriasis is brought about by an overactive resistant framework. Indications incorporate chipping, aggravation, and thick, white, shimmering, or red patches of skin Psoriasis on the stomach of the patient. Psoriasis is brought about by an overactive resistant framework. Side effects incorporate chipping, aggravation, and thick, white, shimmering, or red patches of skin Psoriasis on the hand of the patient. Psoriasis is brought about by an overactive insusceptible framework. Manifestations incorporate chipping, irritation, and thick, white, shimmering, or red patches of skin Psoriasis on the elbow of the patient. Psoriasis is brought about by an overactive insusceptible framework. Side effects incorporate chipping, irritation, and thick, white, shiny, or red patches of skin Psoriasis on the scalp of the patient. Psoriasis is brought about by an overactive resistant framework. Indications incorporate chipping, irritation, and thick, white, shimmering, or red patches of skin Psoriasis on the hand and fingers of the patient. Psoriasis is brought about by an overactive resistant framework. Manifestations incorporate chipping, aggravation, and thick, white, shimmering, or red patches of skin Psoriasis on the scalp of the patient. Scalp psoriasis is brought about by an overactive safe framework. Manifestations incorporate chipping, irritation, and thick, white, shiny, or red patches of skin Psoriasis on the arm and stomach of the patient. Psoriasis is brought about by an overactive invulnerable framework. Indications incorporate chipping, irritation, and thick, white, gleaming, or red patches of skin

Manifestations

The overall indications of psoriasis include:

red, kindled, layered skin patches

layered skin

dryness and irritation

The sorts of psoriasis might be comparative, yet certain indications will contrast between the kinds of psoriasis:

Plaque psoriasis – this can occur in any space of the body, textured, raised, dry, irritated, excruciating, red skin, however these normally occur on the scalp, knees, elbows, and lower back

Nail psoriasis – little nail pits, edges, openings in the nail, yellow tone, the nail disengaging from the nail bed in pieces or totally

Guttate psoriasis – raised, little red, layered spots rather than patches

Pustular psoriasis – white knocks loaded up with discharge encompassed by red blotches

Reverse psoriasis – primarily shows up around the crotch, under the bosoms, armpits, and privates, as a smooth, red patches of excited skin

Erythrodermic psoriasis – extreme redness, tingling, torment, and scaling over an enormous region, brought down internal heat level, fever, quicker heartbeat

Psoriatic joint inflammation – red, textured patches, difficult and swollen joints, tendons, and ligaments

Clinical appearance

Plaque psoriasis: This is the most widely recognized show and ordinarily addresses a more steady infection. The normal injury is a raised, all around divided erythematous plaque of variable size. In untreated illness, a silver/white scale is clear and more clear on scratching the surface, which uncovers draining focuses. This is known as the Auspitz sign. The most well-known locales are the extensor surfaces, remarkably elbows and knees, and the lower back. Others include:

Scalp: association is seen in roughly a little over half of patients. Ordinarily, effectively obvious, erythematous layered plaques are apparent inside the hair-bearing scalp and there is clear boundary at or past the hair edge. The association of the rear of the head is normal and hard to treat. Less frequently, fine diffuse scaling might be available and hard to recognize from seborrheic dermatitis (dandruff incited irritation of the skin). The contribution of different locales like eyebrows, nose, lips, and upper chest, isn't phenomenal. Brief balding can happen however a lasting misfortune is uncommon.

Nails: Psoriatic nail inclusion is described by; Onycholysis (lifting of the nail plate off the nail bed, showing as a white or salmon fix on the nail), Subungual hyperkeratosis (collection of powdery looking material under the nail because of unnecessary cell division of the nail bed that can eventually prompt breakdown of nails), Nail pitting (exceptionally little sorrows in the nail plate which result from loss of extraordinary sort of cells from the nail surface), Beau's lines (cross over lines on the nail plate because of aggravation of the nails prompting a transient capture in nail development), Splinter hemorrhages (which seem as though minute longitudinal dark lines because of spillage of blood from widened convoluted veins).

Guttate psoriasis: Guttate psoriasis comprises of far and wide little plaques dissipated on the storage compartment and appendages. Young people are most regularly influenced and there is frequently a first sensitive throat. There is much of the time a family background of psoriasis. The unexpected beginning and far and wide nature of guttate psoriasis can be extremely disturbing for patients, luckily, it for the most part settle totally, however can be intermittent or envoy the beginning of persistent plaque psoriasis.

Palmoplantar pustular psoriasis (PPPP): PPPP is described by numerous sterile pustules on the palms and soles. Pustules initially show up as yellowish sores that turn an earthy colored tone with chronicity and related scaling. Most patients with PPPP are smokers.

Intense summed up pustular psoriasis: Acute summed up pustular psoriasis is fortunately phenomenal as it is normally a marker of extreme and temperamental psoriasis. Clinically the skin is erythematous and delicate with sheets of sterile pustules, which can create over a couple of hours/days. It could be accelerated by the patient taking steroids. The pustules generally happen at first at the fringe edge of plaques which are frequently sore and erythematous. Pustules in the end dry and the skin desquamates.

Acropustulosis: Acropustulosis is an uncommon variation of psoriasis that generally happens in little youngsters. Here pustules show up around the nails and the fingertips related with energetic aggravation.

Flexural psoriasis: Flexural psoriasis creates clear cut erythematous regions in the armpits, crotch, groove between the bum, underneath the bosoms and skin folds. Scaling is insignificant or missing. It is difficult to recognize it from a contagious contamination. In the event of any uncertainty, the specialist should take an example to recognize such a contamination.

Napkin psoriasis: Napkin psoriasis in kids may give regular psoriatic injuries or a more diffuse erythematous ejection with exudative

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Psoriasis

Psoriasis

What is Psoriasis?

Psoriasis is an immune system skin condition where the resistant framework assaults solid skin cells, yet it likewise invigorates the development of skin cells. It's anything but infectious, and it can occur in different pieces of the body

Psoriasis.

Psoriasis is a constant incendiary, hyperproliferative skin infection. It is described by distinct, erythematous (widened skin veins) layered plaques with white surface scale (fast keratinocyte expansion) of sick skin frequently at locales of minor injury especially influencing extensor surfaces, scalp, and nails, and typically follows a backsliding and dispatching course. As psoriasis is brought about by immunological unsettling influences, it's anything but infectious. Psoriasis influences the skin as well as lead to joint pain (irritation of the joints) in roughly 30% of patients.

There are 7 sorts of psoriasis with plaque psoriasis being the most widely recognized kind of psoriasis:

Plaque psoriasis

Nail psoriasis

Guttate psoriasis

Pustular psoriasis

Converse psoriasis

Erythrodermic psoriasis

Psoriatic joint inflammation

The study of disease transmission of psoriasis

Geology: Around the world 1-2% of the populace is influenced by psoriasis (125 million individuals in the UK/USA/Japan alone). It is less entirely expected in African, South American and Asian populaces; notwithstanding, psoriasis influences roughly 1.5-3% of Caucasians.

Sex and age: Psoriasis influences both genders equitably. It can introduce at whatever stage in life and in excess of half of patients present before the age of thirty years; in spite of the fact that it is seen infrequently before the age of five years. There is a bimodal appropriation old enough of beginning, with the beginning stage kind happening in pre-adulthood and early adulthood. This sort is generally serious in force and patients regularly have a background marked by psoriasis in the family. The later-beginning kind presents between the ages of fifty and sixty, less extreme and is emotional in force. Family ancestry is generally missing in this sort.

Pathophysiology of psoriasis

Both hereditary and natural elements are significant. A youngster who has one parent with psoriasis has a one of every four shot at fostering the sickness. In the event that one indistinguishable (monozygotic) twin has psoriasis, there is a 70% possibility that the other will likewise be influenced; notwithstanding, just a 20% possibility exists in the non-indistinguishable (dizygotic) twins. There is currently huge exploration work showing that psoriasis is additionally connected with other significant comorbidities, for example, type 2 diabetes (expanded danger of 1.4 occasions), sorrow, heftiness, cardiovascular illness, and decreased personal satisfaction. Natural elements include:

Injury: Sores can show up at locales of skin injury, like scratches or careful injuries. This wonder is named the Köbner isomorphic marvel.

Contamination: Throat diseases frequently go before guttate psoriasis. Serious psoriasis might be the underlying show of HIV contamination.

Daylight: Psoriasis may happen or deteriorate after sun openness.

Medications: Numerous medications including antimalarials, β-blockers, lithium, and Non-Steroidal Mitigating Medications (NSAIDs) can intensify psoriasis. Bounce back; flare of psoriasis is regularly flimsy and perhaps pustular and may happen after the withdrawal of steroids.

Mental elements: Nervousness and stress may fuel psoriasis in inclined people.

Our consideration group will assist you with your psoriasis. We realize it tends to be hard to live with psoriasis. With a very long time of face to face and computerized clinical experience treating psoriasis, we realize what works, and at costs that will not burn through every last cent. Try not to spare a moment to be assessed, so we can treat you. One of our online specialists can see you now.  

Psoriasis on the elbow of the patient. Psoriasis is brought about by an overactive safe framework. Manifestations incorporate chipping, irritation, and thick, white, shiny, or red patches of skin Psoriasis on the stomach of the patient. Psoriasis is brought about by an overactive resistant framework. Indications incorporate chipping, irritation, and thick, white, shimmering, or red patches of skin Psoriasis on the hand of the patient. Psoriasis is brought about by an overactive safe framework. Manifestations incorporate chipping, irritation, and thick, white, shiny, or red patches of skin Psoriasis on the elbow of the patient. Psoriasis is brought about by an overactive insusceptible framework. Indications incorporate chipping, aggravation, and thick, white, brilliant, or red patches of skin Psoriasis on the scalp of the patient. Psoriasis is brought about by an overactive invulnerable framework. Indications incorporate chipping, irritation, and thick, white, brilliant, or red patches of skin Psoriasis on the hand and fingers of the patient. Psoriasis is brought about by an overactive resistant framework. Indications incorporate chipping, aggravation, and thick, white, gleaming, or red patches of skin Psoriasis on the scalp of the patient. Scalp psoriasis is brought about by an overactive resistant framework. Indications incorporate chipping, irritation, and thick, white, shimmering, or red patches of skin Psoriasis on the arm and stomach of the patient. Psoriasis is brought about by an overactive invulnerable framework. Side effects incorporate chipping, aggravation, and thick, white, brilliant, or red patches of skin

Side effects

The overall indications of psoriasis include:

red, kindled, layered skin patches

flaky skin

dryness and irritation

The sorts of psoriasis might be comparative, yet certain side effects will contrast between the kinds of psoriasis:

Plaque psoriasis – this can occur in any space of the body, flaky, raised, dry, bothersome, excruciating, red skin, yet these normally occur on the scalp, knees, elbows, and lower back

Nail psoriasis – little nail pits, edges, openings in the nail, yellow tone, the nail confining from the nail bed in pieces or totally

Guttate psoriasis – raised, little red, layered spots rather than patches

Pustular psoriasis – white knocks loaded up with discharge encompassed by red blotches

Converse psoriasis – chiefly shows up around the crotch, under the bosoms, armpits, and privates, as a smooth, red patches of excited skin

Erythrodermic psoriasis – serious redness, tingling, torment, and scaling over an enormous region, brought down internal heat level, fever, quicker heartbeat

Psoriatic joint pain – red, layered patches, excruciating and swollen joints, tendons, and ligaments

Clinical appearance

Plaque psoriasis: This is the most widely recognized show and typically addresses a more steady infection. The average injury is a raised, all around separated erythematous plaque of variable size. In untreated illness, a silver/white scale is clear and more clear on scratching the surface, which uncovers draining focuses. This is known as the Auspitz sign. The most well-known destinations are the extensor surfaces, strikingly elbows and knees, and the lower back. Others include:

Scalp: association is seen in around a little over half of patients. Ordinarily, effectively unmistakable, erythematous layered plaques are obvious inside the hair-bearing scalp and there is clear division at or past the hair edge. The contribution of the rear of the head is normal and hard to treat. Less regularly, fine diffuse scaling might be available and hard to recognize from seborrheic dermatitis (dandruff incited aggravation of the skin). The contribution of different destinations like eyebrows, nose, lips, and upper chest, isn't phenomenal. Impermanent balding can happen however a lasting misfortune is surprising.

Nails: Psoriatic nail association is portrayed by; Onycholysis (lifting of the nail plate off the nail bed, showing as a white or salmon fix on the nail), Subungual hyperkeratosis (collection of pale looking material under the nail because of unreasonable cell division of the nail bed that can eventually prompt breakdown of nails), Nail pitting (exceptionally little dejections in the nail plate which result from loss of uncommon sort of cells from the nail surface), Lover's lines (cross over lines on the nail plate because of irritation of the nails prompting a transient capture in nail development), Splinter hemorrhages (which appear as though minute longitudinal dark lines because of spillage of blood from widened convoluted veins).

Guttate psoriasis: Guttate psoriasis comprises of broad little plaques dispersed on the storage compartment and appendages. Young people are most generally influenced and there is regularly a previous sore throat. There is every now and again a family background of psoriasis. The abrupt beginning and inescapable nature of guttate psoriasis can be exceptionally disturbing for patients, luckily, it normally settle totally, however can be repetitive or envoy the beginning of constant plaque psoriasis.

Palmoplantar pustular psoriasis (PPPP): PPPP is described by different sterile pustules on the palms and soles. Pustules initially show up as yellowish injuries that turn an earthy colored tone with chronicity and related scaling. Most patients with PPPP are smokers.

Intense summed up pustular psoriasis: Intense summed up pustular psoriasis is fortunately exceptional as it's anything but a pointer of extreme and insecure psoriasis. Clinically the skin is erythematous and delicate with sheets of sterile pustules, which can create over a couple of hours/days. It could be accelerated by the patient taking steroids. The pustules ordinarily happen at first at the fringe edge of plaques which are frequently sore and erythematous. Pustules at last dry and the skin desquamates.

Acropustulosis: Acropustulosis is an uncommon variation of psoriasis that generally happens in little youngsters. Here pustules show up around the nails and the fingertips related with energetic aggravation.

Flexural psoriasis: Flexural psoriasis creates distinct erythematous regions in the armpits, crotch, groove between the rump, underneath the bosoms and skin folds. Scaling is insignificant or missing. It is difficult to recognize it from a contagious contamination. In the event of any uncertainty, the specialist should take an example to identify such a contamination.

Napkin psoriasis: Napkin psoriasis in kids may give regular psoriatic injuries or a more diffuse erythematous ejection with exudative

Comments

[vedas124]

Psoriasis

Psoriasis is an immune system skin condition where the resistant framework assaults sound skin cells, yet it likewise animates the development of skin cells. It's anything but infectious, and it can occur in different pieces of the body. 

Psoriasis is an ongoing provocative, hyperproliferative skin sickness. It is described by distinct, erythematous (expanded skin veins) textured plaques with white surface scale (fast keratinocyte multiplication) of infected skin regularly at locales of minor injury especially influencing extensor surfaces, scalp, and nails, and as a rule follows a backsliding and dispatching course. As psoriasis is brought about by immunological unsettling influences, it's anything but infectious. Psoriasis influences the skin as well as lead to joint inflammation (irritation of the joints) in roughly 30% of patients. 

The study of disease transmission of psoriasis 

1- Topography: Globally 1-2% of the populace is influenced by psoriasis (125 million individuals in the UK/USA/Japan alone). It is less entirely expected in African, South American and Asian populaces; in any case, psoriasis influences roughly 1.5-3% of Caucasians. 

2- Sex and age: Psoriasis influences both genders equitably. It can introduce at whatever stage in life and in excess of half of patients present before the age of thirty years; in spite of the fact that it is seen once in a while before the age of five years. There is a bimodal circulation old enough of beginning, with the beginning stage kind happening in immaturity and early adulthood. This sort is generally serious in power and patients frequently have a past filled with psoriasis in the family. The later-beginning kind presents between the ages of fifty and sixty, less serious and is emotional in force. Family ancestry is normally missing in this sort.

[digitalyogesh]

Psoriasis

Psoriasis is an immune system skin condition where the insusceptible framework assaults solid skin cells, however it likewise animates the development of skin cells. It’s anything but infectious, and it can occur in different pieces of the body.

Psoriasis is a persistent fiery, hyperproliferative skin sickness. It is portrayed by obvious, erythematous (widened skin veins) flaky plaques with white surface scale (quick keratinocyte multiplication) of sick skin regularly at locales of minor injury especially influencing extensor surfaces, scalp, and nails, and ordinarily follows a backsliding and dispatching course. As psoriasis is brought about by immunological unsettling influences, it’s anything but infectious. Psoriasis influences the skin as well as lead to joint inflammation (irritation of the joints) in roughly 30% of patients.

There are 7 kinds of psoriasis with plaque psoriasis being the most widely recognized sort of psoriasis:

Plaque Psoriasis

Nail psoriasis

Guttate psoriasis

Pustular psoriasis

Converse psoriasis

Erythrodermic psoriasis

Psoriatic joint inflammation

The study of disease transmission of psoriasis

Geology: Globally 1-2% of the populace is influenced by psoriasis (125 million individuals in the UK/USA/Japan alone). It is less entirely expected in African, South American and Asian populaces; be that as it may, psoriasis influences around 1.5-3% of Caucasians.

Sex and age: Psoriasis influences both genders equitably. It can introduce at whatever stage in life and in excess of half of patients present before the age of thirty years; despite the fact that it is seen once in a while before the age of five years. There is a bimodal dissemination old enough of beginning, with the beginning stage kind happening in immaturity and early adulthood. This sort is typically serious in force and patients frequently have a background marked by psoriasis in the family. The later-beginning kind presents between the ages of fifty and sixty, less extreme and is sensational in force. Family ancestry is generally missing in this sort.

Pathophysiology of Psoriasis

Both hereditary and ecological components are significant. A youngster who has one parent with psoriasis has a one of every four shot at fostering the infection. In the event that one indistinguishable (monozygotic) twin has psoriasis, there is a 70% possibility that the other will likewise be influenced; notwithstanding, just a 20% possibility exists in the non-indistinguishable (dizygotic) twins. There is presently huge examination work showing that psoriasis is additionally connected with other significant comorbidities, for example, type 2 diabetes (expanded danger of 1.4 occasions), misery, weight, cardiovascular infection, and diminished personal satisfaction. Natural variables include:

Injury: Lesions can show up at locales of skin injury, like scratches or careful injuries. This marvel is named the Köbner isomorphic wonder.

Contamination: Throat diseases frequently go before guttate psoriasis. Serious psoriasis might be the underlying show of HIV disease.

Daylight: Psoriasis may happen or deteriorate after sun openness.

Medications: Many medications including antimalarials, β-blockers, lithium, and Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) can worsen psoriasis. Bounce back; flare of psoriasis is frequently insecure and perhaps pustular and may happen after the withdrawal of steroids.

Mental variables: Anxiety and stress may fuel psoriasis in inclined people.

Our consideration group will assist you with your psoriasis. We realize it tends to be difficult to live with psoriasis. With a very long time of face to face and advanced clinical experience treating psoriasis, we understand what works, and at costs that will not burn through every last dollar. Try not to stop for a second to be assessed, so we can treat you. One of our online specialists can see you now.

Photographs

Psoriasis on the elbow of the patient. Psoriasis is brought about by an overactive insusceptible framework. Side effects incorporate chipping, irritation, and thick, white, shiny, or red patches of skin Psoriasis on the stomach of the patient. Psoriasis is brought about by an overactive invulnerable framework. Indications incorporate chipping, aggravation, and thick, white, brilliant, or red patches of skin Psoriasis on the hand of the patient. Psoriasis is brought about by an overactive safe framework. Manifestations incorporate chipping, aggravation, and thick, white, gleaming, or red patches of skin Psoriasis on the elbow of the patient. Psoriasis is brought about by an overactive resistant framework. Manifestations incorporate chipping, irritation, and thick, white, shiny, or red patches of skin Psoriasis on the scalp of the patient. Psoriasis is brought about by an overactive invulnerable framework. Side effects incorporate chipping, aggravation, and thick, white, shimmering, or red patches of skin Psoriasis on the hand and fingers of the patient. Psoriasis is brought about by an overactive safe framework. Manifestations incorporate chipping, irritation, and thick, white, gleaming, or red patches of skin Psoriasis on the scalp of the patient.

Scalp Psoriasis is brought about by an overactive resistant framework. Manifestations incorporate chipping, irritation, and thick, white, gleaming, or red patches of skin Psoriasis on the arm and stomach of the patient. Psoriasis is brought about by an overactive invulnerable framework. Manifestations incorporate chipping, irritation, and thick, white, brilliant, or red patches of skin

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Lupine Publishers | Micro-Environmental Systems and Endothelial Cells in Cooperative Tumorigenesis Account for Potential Malignant Transformation in Neurofibromatosis Type 1 Patients

Lupine Publishers |  Open Access Journal of Oncology and Medicine (OAJOM)

Abstract

Overall tumorigenesis in neurofibromatosis type 1 patients constitutes a series of specific targeting events with a central role enacted by proliferation of fibroblasts and endothelial cells in overproduction of growth factors and cytokines such as transforming growth factor-beta and CXCL12 cytokine. The plexiform neurofibroma well-illustrates dimensions of such cooperative participation within operative fields of the initial Schwann cell proliferation leading in a significant number of patients to malignant transformation of the peripheral nerve sheath tumors. Inclusive directions in operative targeting of Schwann cells or astrocytes are staged performance in the transformation of hyperproliferative induction and constitute further evolutionarily defined incorporation of such systems as endothelial cells. Hyperproliferative cell subsets are initial and also consequential target formulation of potential malignant states as induced in malignant peripheral nerve sheath tumors.

Introduction

Neurofibromatosis type 1 (NF1) is a neurogenetic disorder and involves both heterozygous and homozygous absence/reduction of neurofibromin that acts normally as a tumor suppressor. There is a need to assess predisposing genetic factors and loss of heterozygosity causing emergence of aggressive neoplasms in patients with NF1 [1]. The two hit hypothesis helps account for the emergence of Schwann cell-based proliferations and for neurofibromas and plexiform neurofibromas. Gherkin may act on tumorigenesis of cutaneous neurofibromas via growth hormone secretagogue receptor [2]. It is important to consider the neurofibroma that is based on micro-environmental potentiation of tumor generation in patients that develop malignant nerve sheath tumors and astrocytomas in patients with NF1 +/- genotype; this occurs in a manner that involves growth factor overactivity and mast cell and endothelial overactivity within a milieu that dysfunctionally stimulates tumorigenesis. Reactive oxygen species overproduction lead to epithelial-mesenchymal transit in patients with neurofibromin deficiency and plays a crucial role in NF1 tumor growth [3]. RAS activation alone is not sufficient for malignant transformation of peripheral nerve sheath tumors; signal transduction may potentially help identify therapies for this neoplasm type [4].

Neurofibromin

The dynamics of neurofibromin as a cytoplasmic protein involve the regulation of K-Ras, and the PI3K/Akt pathways; absence of neurofibromin leads to overactivation of these pathways in various ways in inducing tumorigenesis in such lesions as optic tract pilocytic astrocytomas, brain stem astrocytomas and also other CNS astrocytomas in terms of progression of these lesions. The cell of origin determines the temporal course of neurofibromatosis-1 low-grade glioma formation [5]. The micro-environment of plexiform neurofibromas of peripheral nerves and of nerve plexi include a 10% risk of malignant change with subsequent aggressive clinical behavior in the affected patients. Over expression of cellular retinoid acid binding protein 2 is reported in several cancer types, including malignant peripheral nerve sheath tumors (MPNSTs) [6].

Related Tumor Predispositions

The neurofibromin insufficiency status in Schwann cells and fibroblasts allows for enhanced participation of immune system component cells such as microglia as evidenced in optic pathway low-grade astrocytomas. Telomere erosion is described in many tumor types and may potentially drive genomic instability and clonal progression in NF1-associated MPNSTs [7]. Tumor dimensions include proliferation of astrocytic cells in optic pathways, and of various subtypes of stromal cells such as fibroblasts and mast cells in the peripheral nervous system. It is significant to consider particularly the micro-environmental active participation in the genesis of the most common tumor type in Neurofibromatosis type 1 patient, that is the neurofibroma, which invokes proliferation of fibroblasts and endothelial cells. The congenital plexiform neurofibroma is in fact a hypervascular lesion that transgresses tissue margins and induces a significant risk for malignant transformation. NF1 loss is the primary driver of tumorigenesis in neurofibromatosis type 1-related plexiform neurofibroma [8]. It is further to such considerations that important cooperative intervention in malignant transformation of plexiform neurofibromas invokes multi-type cells in inducing proliferation of an integral Schwann cell-fibroblastic twin population in enhancing potential malignant transformation of the peripheral nerve sheath. A therapeutic window for neuroprotective intervention exists as detected by optical coherence tomography in mice with optic glioma, and particularly as an accurate biomarker of retinal ganglion cell apoptosis [9]. The heterozygous absence of one neurofibromin allele in mice results in plexiform neurofibromas and low-grade optic pathway astrocytomas. Mast cells appear to play a causal role in neurofibroma formation and also in microglia in optic pathway glioma evolution [10]. Such implications of the micro-enviromental factors includes a distinctive cooperative participation that carries implications for significant enhancement of cell proliferation and of such cytokines such as transforming growth factor and CXCL12 in formulating malignant transformation in such tumors. The methylemetetrahydrofolate reductase 1298 and 677 gene polymorphisms are related to optic glioma and hamartoma risk in NF1 patients through effects on DNA synthesis and methylation [11].

Convergent Targeting

The related tuberous sclerosis complex is analogous to neurofibromatosis type 1 as a neurogenetic disorder associated with increased risk for astrocytomas in the form of subependymal giant cell astrocytomas. A convergent targeting of systems of cell proliferation include in particular cyclic AMP and Ras in a manner that includes dimensions of micro-environmental conditioning. Mutations of the NF 1 gene are frequent in many cancer types in patients without NF1 and this is suggestive of a more general role for the NF1 gene in oncogenesis. In melanoma NF1 mutations potentially drive tumorigensis and promote drug resistance [12]. Inclusive dynamics allow for permissive tumorigenesis in a manner that includes the incorporation of malignant transformation within confines of a Schwann cell-fibroblast-endothelial cell system in the case of malignant peripheral nerve sheath tumors. Astrocytes and microglia are analogous counterparts in the induction of CNS astrocytomas. Such considerations are inclusive phenomena of multi-component induction of potential malignancy that recharacterizes conditioning of the micro-environment of proliferative states preceding tumorigenesis. Interaction between neoplastic Schwann cells and their surrounding neural microenvironment has important implications for early cellular events promoting tumorigenesis in neurofibroma development [13].

Performance Dynamics

Performance dynamics of tumors in neurofibromatosis type 1 may potentially modify the biologic significance of a two-hit hypothesis in a manner that implicates micro-environmental conditioning of the resultant cell hyperplasias and proliferations in such lesions as peripheral nerve sheath tumors and astrocytomas. NF1 provides unique vantage points to examine co-contributions of molecular, cellular, and tissue processes in tumor biology [14]. Such proposed dimensions invoke in particular an over-activation in production and action of growth factors that provoke selective malignant transformation of hyper-proliferative lesions composed of Schwann cells and astrocytes in the peripheral and central nervous systems respectively. Plasma soluble levels of transforming growth factor-beta and interleukin-6 are increased in NF1 patients and a shift towards an anti0inflammatory profile has been reported in cells expressing cytokines [15].

Hyperproliferation

The hyperproliferative states affecting Schwann cells and astrocytes invoke also fibroblast and microglial cell proliferations in a manner transforming tumorigenesis. Such facilitation to tumorigenesis invokes dimensions of transformation as well seen in plexiform neurofibromas that may undergo malignant transformation in a significant number of affected individuals. Such considerations are selective targeting of specific cell subpopulations in a manner that allows permissive transformation. Insertional mutagenesis identifies a STAT3/Arid1b/beta-catenin pathway that drives neurofibroma initiation in the context of Nf1 loss [16]. Mast cells and fibroblasts may potentially incorporate endothelial cells that may participate as central dysregulatory dimensions in plexiform neurofibroma tumorigenesis. The provocations for malignant transformation further cooperate in systems of derivative consequence as hypervascular lesions that subsequently lead to potential malignant cells in individual patients. Cross species comparative oncogenomic may identify driver mutations in mouse cancer models and allow validation in human tumors [17].

Concluding Remarks

Propositional implications in tumorigenesis include the multi-component participation of Schwann cells on the one hand and of fibroblasts, mast cells, endothelial cells and also of microglia in an inductive process that includes specific pathways of malignant transformation. Endothelial cell proliferation is related to substantial participation in modes related to key-events of increased proliferation of Schwann cells and astrocytes in initial stages of lesion infliction. Inclusive phenomena have thus become systems of consequence in affecting such specific cell proliferative states. Such events occur within the added dimensions of directed targeting of multiple-agent micro environmental modeling of the initial proliferation of the Schwann cells or astrocytes. A pivotal series of roles played by fibroblasts, endothelial cells, mast cells and of microglia and astrocytes appears a dynamic milieu within added consequences of malignant transformation of both Schwann cells and astrocytes that progress as cooperative systems of tumorigenesis.

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Benefits and Uses of Horsetail (Shavegrass)

New Post has been published on https://healingawerness.com/news/benefits-and-uses-of-horsetail-shavegrass/

Benefits and Uses of Horsetail (Shavegrass)

I’ve been using herbs and herbal preparations for years now to treat mild issues at home. Horsetail (also called shavegrass) is an herb that I always keep in the herb cabinet (which is what I have instead of a medicine cabinet!). It has been my go-to for hair, skin, and nail health but I am still learning that there are even more benefits and uses of horsetail herb.

What Is Horsetail?

Horsetail (Equisetum arvense) is a medicinal plant used for remedies that dates back to ancient Greek and Roman civilizations. But it has been around much longer, as early as before the dinosaurs. Prehistoric horsetail was much taller, the size of a tree, but today’s horsetail reaches just about 4 feet tall. Horsetail is thought to be the most abundant source of silica in the plant kingdom. Because of this, it has been used in the past to polish metal.

The above-ground part of the plant is what is used for herbal medicine. It has been used traditionally for many ailments and to support natural health:

Hair, bone, nail, and skin health

Mouth and throat health

Healing wounds

Viral infections

Digestion help

Cardiovascular and respiratory ailments

Bladder problems (including bed-wetting)

Bleeding issues

Immune system support

While herbalists have used horsetail for traditional remedies for many years, there isn’t a lot of scientific data to support its use. However, the small amount of research that is available is promising and makes a case for further research.

Horsetail Benefits

Horsetail has many uses in traditional herbal medicine. Science is also beginning to back up these claims. Here are some of the most common benefits of horsetail:

High in Nutrients and Antioxidants

One of the most interesting benefits of horsetail is how nutrient dense it is. Horsetail contains the following nutrients:

Horsetail also contains Kynurenic acid, which reduces inflammation and pain, as well as silica, which supports collagen production. It also contains chlorophyll, known to fight cancer by preventing the cytotoxic and hyperproliferative effects of iron metabolism.

Additionally, research suggests that horsetail has antioxidant properties and may even inhibit cancer cell growth because of this.

Promotes Bone Health

The high level of silica in horsetail is one of its main health benefits. Silica is important for bone and teeth health among other things. In a 1999 study, post-menopausal women with osteoporosis regained significant bone density after 1 year of supplementation of horsetail.

Fights Illness and Infection

Traditional herbalists use horsetail on wounds, especially boils and carbuncles. It turns out this use is scientifically backed. Horsetail has antimicrobial and anti-inflammatory properties that help with disease and infection. One 2006 study tested horsetail essential oil on a number of bacteria and fungi like Staph, Salmonella, and Candida. It was found to have a broad spectrum effect on all strains tested.

Has Diuretic Properties

Horsetail has been used traditionally as a diuretic and to treat bladder issues for centuries. A 2014 study found that horsetail works as well as a conventional diuretic medicine (hydrochlorothiazide) without side effects such as significant changes to liver or kidney function or electrolyte balance.

Additionally, many diuretic drugs cause electrolyte issues but this study found that horsetail does not cause the same issues. This may be because horsetail is also a good source of electrolytes.

Supports Hair, Skin, and Nail Health

Horsetail has also been used traditionally for hair, skin, and nail health. It’s thought that the high silica content of horsetail is the reason why it works. Silica helps boost collagen production which is important for healthy hair, skin, and nail.

Science backs this up too. A 2016 study found that hair with high amounts of silica was less likely to fall out and was also more lustrous than hair with lower levels of silica.

Horsetail can even help regrow hair after hair loss. According to this 2012 study, significant hair growth occurred after 90 and 180 days of supplementing with horsetail herb.

One study published in the Journal of Plastic Dermatology found that using horsetail topically on nails reduced splitting and fragility of nails as well as reduced longitudinal grooves.

Additionally, a 2015 study found horsetail ointment helped heal episiotomy wounds and reduced pain associated with it.

Horsetail Uses

I often use this herb, especially in external preparations due to its skin/hair supportive high silica content:

Increase bone density – Take a supplement of horsetail with calcium daily.

As an herbal hair rinse – I brew a strong herbal tea (1/2 cup horsetail to 1 cup water), steep for an hour, strain and use as a hair rinse in the shower.

For boils and blisters – I grind the dried herb with plantain and add enough water to create a paste and then pack on to boils or blisters and cover with gauze to speed healing.

For nails – Use horsetail oil on nails to improve strength and reduce breakage and splitting.

As diuretic – Drink horsetail tea to remove excess water.

Sore throat – For sore throat, I make a gargle with a strong horsetail infusion (steeping horsetail in boiling water and then cooling) with sea salt and lemon juice and then gargle with this mixture a few times a day while symptoms persist.

Bedwetting/bladder problems – A capsule of horsetail extract two or three times daily may be helpful for alleviating some of the symptoms of bladder and urinary tract infections (although not necessarily solving the problem, see this post on UTIs), incontinence, and even bed wetting because it can relieve the urge to urinate. Or try a bath in horsetail tea (steep dried horsetail in a quart of boiling water for 10-15 minutes and then strain and add to bath).

Is Horsetail Safe? Additional Notes

I avoid this herb when pregnant or nursing (so my whole married life!) but use it externally for hair or skin if needed.

Precautions for using horsetail include:

Drink lots of water while taking horsetail

Don’t take if you have a kidney problem

Check with your doctor if you take medications as some may interact with horsetail (including causing potassium imbalance)

Horsetail may lower blood glucose so diabetics should check with their doctor before use

Because it contains traces of nicotine, horsetail is not recommended for children

Pregnant and breastfeeding women should avoid horsetail as there aren’t any safety studies

Choose a thiaminase-free formula as thiaminase can block absorption of thiamine

Otherwise, horsetail is generally considered safe when taken in short-term use.

Where to Buy Horsetail Root

There are many places you can purchase it from online, and possibly even locally, but I typically buy it here and make it as a tea. This powdered version is a little more convenient you don’t have to steep or strain it. You can also try capsule form, although I haven’t personally.

You can also grow your own horsetail. If you want to try it, start with it in a container since it spreads very easily and may take over your garden!

Have you ever used horsetail? How did you use it? Tell me below!

Sources:

De vogel J, Jonker-termont DS, Van lieshout EM, Katan MB, Van der meer R. Green vegetables, red meat and colon cancer: chlorophyll prevents the cytotoxic and hyperproliferative effects of haem in rat colon. Carcinogenesis. 2005;26(2):387-93.

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[pharmaphorumuk]

The Problem of the Hyperprolific Author When It Comes to KOL Identification

When identifying KOLs, it’s both common and correct to include “publications” as one of the identification and screening criteria.

But it’s worth remembering the dangers of an over-reliance on publication data, especially in the context of hyper-prolific authors.

We all know that the top publishers in a therapy area are not always the top KOLs for a variety of reasons.

But the wariness of “top publishers” should also extend to authors who publish a very high number of papers.

A few years ago, we published our research on this in our paper “Too much of a good thing? An observational study of prolific authors”, by Elizabeth Wager PhD (Sideview), Sanjay Singhvi MBA (System Analytic), and Sabine Kleinert MRCP (The Lancet).

And more recently, a paper in Nature (which also cited our original work) identified implausibly prolific authors and then reached out to them asking for their insights.

All of this continues to support our two key messages when it comes to the role of publications in identifying KOLs:

Always consider the potential negative value of common publication metrics (e.g. number of publications in a year) when trying to identify or characterise KOLs/Experts

Beware the biases created by quant-heavy databases that treat publications as their primary methodology for identifying KOLs.

Omabuwa Tetsola

Services & Innovations

+44 (0)20 3951 0246

omabuwa.tetsola@systemanalytic.com

www.systemanalytic.com

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