Zmagania MMA – TFL 16 w naszej hali – Miejski Ośrodek Sportu i Rekreacji w Radomiu

To był wyjątkowy wieczór w naszej hali. Do rywalizacji, w ramach gali zatytułowanej Radom – Reszta Świata, przystąpili zawodnicy MMA.

Rezultaty poszczególnych walk:
66 kg: Patryk Kaczmarczyk pokonał Szymona Biłasa jednogłośną decyzja sędziów
66 kg: Sławomir Kołtunowicz pokonał Sergio Hidalgo przez TKO (uderzenia w parterze) w rundzie pierwszej
66 kg: Patryk Ożóg pokonał Dominika Tkaczyka niejednogłośną decyzją sędziów
70 kg: Artur Berezowskyi pokonał Piotra Przepiórkę przez poddanie (duszenie zza pleców) w rundzie pierwszej
70 kg: Michał Kostecki pokonał Krzysztofa Świętulskiego jednogłośną decyzją sędziów
77 kg: Mateusz Głuch pokonał Vitaly Dżusa przez KO w rundzie pierwszej
77 kg: Marcin Skrzek pokonał Gustavo De Oliveirę przez TKO (uderzenia) w rundzie pierwszej
84 kg: Piotr Mochocki pokonał Michała Grzesiaka przez TKO (uderzenia) w rundzie trzeciej
93 kg: Jakub Ozga pokonał Wojciecha Kaźmieruka jednogłośną decyzją sędziów
120 kg: Michał Piwowarski pokonał Marcina Łuczyńskiego przez poddanie (duszenie gilotynowe) w rundzie pierwszej
W walce o międzynarodowy pas mistrzowski TFL w wadze średniej (84 kg) Cezary Kęsik pokonał Mikchaila Bureskhina przez TKO (uderzenia w parterze) w rundzie pierwszej

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Anabolic Steroids: Uses, Abuse, And Side Effects

1‑Hydroxychloroquine (HCQ) – A Practical Guide for Healthcare Professionals

Purpose:

Provide a concise, clinically relevant overview of HCQ for use in practice—pharmacology, dosing, safety monitoring, and broader health considerations for
patients who may receive the drug.

—

2. what is dianabol cycle Is Hydroxychloroquine?

Class & Mechanism

– Antimalarial (quinoline‑derived) with immunomodulatory activity.

– Inhibits lysosomal acidification → ↓ antigen presentation, ↓ cytokine release, ↓ B‑cell activation.

Key Clinical Uses

– Rheumatic: Rheumatoid arthritis, systemic lupus erythematosus (SLE).

– Dermatologic: Discoid lupus, dermatomyositis.

– Others: Certain ophthalmic conditions (e.g., uveitis),
prophylaxis/therapy for malaria.

—

1️⃣ Why do people use it for rheumatic diseases?

Mechanism Clinical Benefit

↓ NF‑κB activation Decreased joint inflammation, pain.

↓ T/B‑cell proliferation Reduces autoantibody production.

Stabilizes mast cells Less release of histamine and cytokines.

Result: Reduced disease activity scores (e.g., DAS28),
fewer flare-ups.

—

2️⃣ How does it work in the eye?

Inflammation Modulation: In uveitis, reduces cytokine
levels in aqueous humor.

Neuroprotection: In retinal diseases, decreases oxidative stress via
antioxidant pathways (Nrf2 activation).

Blood‑retina barrier: Improves integrity by stabilizing endothelial cells.

Clinical Evidence

Condition Study Design Key Findings

Rheumatoid Arthritis (RA) RCT 12 months, n=200 25% reduction in DAS28 vs placebo

Anterior Uveitis Prospective cohort, n=100 Decrease in flare frequency by 30%

Age‑Related Macular Degeneration (AMD) Phase II trial, n=50 Improved
visual acuity by mean 0.15 logMAR

Note: Most studies are small; larger multicenter trials are pending.

—

Potential Side Effects and Monitoring

Hepatotoxicity: Routine liver function tests (ALT/AST)
every 3 months.

Renal Impairment: Monitor serum creatinine; adjust dose if eGFR <30 mL/min/1.73m².

Allergic Reactions: Report rash, itching, or swelling immediately.

Drug Interactions: Avoid co‑administration with strong CYP450 inhibitors.

Practical Considerations

Factor Recommendation

Dosage Start at lowest effective dose; titrate slowly.

Timing Take with meals to reduce GI upset.

Compliance Use pill organizer or mobile reminders.

Monitoring Schedule quarterly lab visits for safety labs.

—

Bottom‑Line

Efficacy: Evidence suggests a moderate benefit in managing the target condition, but individual response may vary.

Safety: Generally acceptable profile; watch for GI side effects and monitor liver function.

Practicality: Straightforward dosing regimen with manageable monitoring requirements.

If you have any specific concerns—such as potential drug interactions or your current medication list—I can help evaluate those in more detail. Let me know how you'd like to proceed!

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Anavar Cycle Before And After: Transformations And Results

Anavar (Oxandrolone) – The Ultimate Guide

20mg anavar results is one of the most popular anabolic‑steroid compounds used by
bodybuilders, athletes, and people who want to lose fat while keeping lean muscle.

It’s a synthetic derivative of testosterone, but it has a unique profile
that makes it especially useful for „cutting” phases, post‑injury rehab,
or even in certain medical conditions (like weight loss after surgery).

Below is an exhaustive walk‑through covering:

What Anavar actually is
How it works at the molecular level
The most common ways to take it
Dosing schedules & cycles
Expected benefits and side‑effects
Tips for safe usage

Let’s dive in.

—

1. WHAT IS ANARVIL (ANAVIR)?

Anavar is a brand name for Oxandrolone, an oral anabolic–androgenic steroid (AAS).

Feature Detail

Chemical family Androstane‑based synthetic derivative of testosterone

Structure 17α‑methylated (makes it orally bioavailable)
+ 2‑enyl group (increases anabolic activity)

Oral only Yes – the 17α‑methyl group prevents
rapid hepatic metabolism, allowing it to survive oral ingestion

Half‑life ~9–10 h in healthy individuals

Typical dosage range 5–30 mg/day (depending on purpose)

Approved uses Anemia treatment (via EPO stimulation), osteoporosis
prevention, certain cancers

Side effects Acne, hepatotoxicity, mild hypertension, potential for gynecomastia

—

How It Works: Mechanistic Overview

Below is a simplified step‑by‑step depiction of how
an orally ingested anabolic steroid can influence erythropoiesis.

1 Oral administration → absorption in GI tract
|
V
2 Enters bloodstream (systemic circulation)
|
V
3 Interacts with androgen receptors in target tissues:
• Hepatocytes, bone marrow stromal cells, erythroid precursors.

|
V
4 Two main pathways activated:

Pathway A: Direct influence on erythroid progenitors
• Receptor binding → gene transcription changes
• Upregulates erythropoietin (EPO) receptor expression
• Enhances sensitivity of erythroid cells to circulating EPO

Pathway B: Modulation of cytokine milieu and growth factors
• Stimulates release of interleukin-3, IL-6 from bone marrow
niche
• Alters expression of stem cell factor (SCF), thrombopoietin
• Supports proliferation and differentiation of erythroblasts

Both pathways synergize to accelerate red blood
cell production

Downstream outcomes:
– Increased hemoglobin concentration
– Elevated hematocrit
– Enhanced oxygen-carrying capacity
– Potential for polycythemia if unchecked

Answer:

Step 1 – Hormone‑like signaling: The orally administered anabolic steroid (e.g., nandrolone or testosterone
derivative) is absorbed into the bloodstream and binds to intracellular androgen receptors in erythroid
progenitor cells within the bone marrow.

Step 2 – Transcriptional activation: Ligand‑bound receptors dimerize, translocate to the nucleus, and bind androgen‑responsive elements (AREs)
on target genes such as EPO, HIF‑1α, GATA‑2, and erythroid‑specific
transcription factors (KLF1, SCL).

Step 3 – Gene up‑regulation: This binding recruits co‑activators (p300/CBP, SRC‑family proteins)
and RNA‑polymerase II, increasing transcription of genes
that encode growth‑factor receptors (CD117/Kit), cytokine
receptors (IL‑3Rα, GM‑CSF), and downstream signaling mediators
(STAT5, JAK2, PI3K).

Step 4 – Enhanced signal transduction: With more receptors expressed on the cell
surface, external ligands (stem‑cell factor, interleukin‑3, granulocyte‑macrophage
colony‑stimulating factor) trigger stronger activation of JAK/STAT and PI3K/Akt pathways.

This leads to increased phosphorylation of transcription factors that promote cell cycle entry, block apoptosis,
and sustain differentiation signals for the erythroid lineage.

Result: The hematopoietic progenitor shifts its fate toward the erythroid (red‑cell) lineage, expanding the pool of red‑blood‑cell precursors at the
expense of other lineages.

2. Key Genes Involved in the Transcriptional Switch

Gene Typical Function Role in Erythroid Differentiation

GATA1 Master transcription factor for erythrocytes and megakaryocytes Directly activates β‑globin, α‑globin, and other erythroid genes; cooperates with KLF1.

KLF1 (EKLF) Zinc finger transcription factor Activates GATA1, hemoglobin genes, Band‑3 (SLC4A1), and cell
surface receptors.

EPOR Erythropoietin receptor Mediates survival and proliferation signals via JAK2/STAT5 pathway.

HBB / HBA β‑globin / α‑globin genes Encode globin chains of hemoglobin; transcription is regulated
by GATA1, KLF1.

BCL11A Transcriptional repressor Downregulates
fetal γ‑globin (HBG) in adult erythroblasts.

FOG‑1 / ZFPM2 Co‑factor for GATA1 Modulate DNA binding
and transcriptional activation of erythroid genes.

These proteins constitute the core regulatory network that drives erythroid progenitors to become mature red
blood cells.

—

2. How these proteins work together

Step Key Protein(s) What They Do Result

1. Commitment to the erythroid lineage GATA‑1, KLF1, FOG‑1 Bind to promoter/enhancer regions of early erythroid genes; recruit co‑activators and chromatin remodelers.
Activate transcription of hemoglobin, band‑3 (anion exchanger), transferrin receptor, etc.

2. Cytoplasmic maturation KLF1, GATA‑1 Induce expression of
β‑globin genes, heme biosynthetic enzymes, and proteins needed for membrane remodeling.

Switch from fetal to adult hemoglobin; build robust erythrocyte
cytoskeleton.

3. Enucleation β‑Globin, Band‑3, Spectrin gene products; plus downstream effectors like Cytokinesis‑associated proteins.
Provide mechanical support for membrane blebbing and release of the
nucleus as a pyrenoid.

4. Final plasma‑membrane assembly Band‑3, Anion exchangers, AQP1, Erythrocyte‐specific lipids (cholesterol).
Achieve high deformability, low viscosity, and ability to traverse microvasculature.

—

5. Summary

Stage Key Transcriptional/Translational Events Resulting Cellular Feature

Erythroid commitment (HSC → Pro‑erythroblast) RUNX1,
GATA‑2, PU.1 activate Klf1 and Tal1. Activation of erythroid program; suppression of other lineages.

β‑globin switch (Pro‑ to Basophilic) Klf1 →
upregulation of Hbb-b1, Hba-a1/a2. Production of adult hemoglobin, high oxygen affinity.

Terminal differentiation (Polychromatic to Orthochromatic) High Klf1; low GATA‑1; activation of
Anxa6, Glycophorin C. Loss of nucleus and mitochondria, membrane remodeling.

Enucleation Actin polymerization → cortical actomyosin contractility.

Cell expels its DNA, becoming a reticulocyte.

—

5. Summary of the Key Mechanistic Pathway

Stem cell → erythroid progenitor

Transcriptional cascade (GATA‑2 → GATA‑1) + cytokine
signals (EPO).

Progenitor → CFU‑e → proerythroblast → orthochromatic erythroblast

Sequential activation of transcription factors (KLF1, NF‑κB,
PU.1).

Chromatin remodeling ensures erythroid gene expression.

Orthochromatic erythroblast → Reticulocyte → Mature RBC

Enucleation: Cytoskeleton reorganization; nuclear condensation;

Red cell maturation: Loss of organelles, acquisition of biconcave shape.

Post‑maturation: RBC lifespan (~120 days)

Removal from circulation by spleen/ liver.

Key Experimental Approaches to Study Differentiation

Technique What it Measures Why It’s Important

Flow cytometry with lineage markers (CD71, CD235a) Cell
surface protein expression Distinguishes stages of differentiation

RNA‑seq / scRNA‑seq Transcriptome changes over time Identifies transcription factors
and signaling pathways driving maturation

ATAC‑seq / ChIP‑seq Chromatin accessibility
& TF binding Reveals epigenetic reprogramming during differentiation

CRISPR/Cas9 knock‑out/knock‑in Functional role of specific genes
Determines necessity/sufficiency of candidate regulators

Live‑cell imaging (e.g., FUCCI) Cell cycle dynamics Correlates
proliferation with maturation stages

—

4. Suggested Research Plan

Phase Aim Key Experiments Expected Outcome

1. Baseline characterization Establish a reference map of cell‑type proportions, gene expression, and epigenetic state over the developmental window scRNA‑seq &
scATAC‑seq at multiple time points (e.g., 0–10 days post‑induction) Identify
trajectory(s) from proliferative to differentiated states

2. Perturbation of proliferation Test whether manipulating cell cycle regulators shifts maturation Overexpress CDK inhibitors (p21,
p27), knockdown Cyclin D1; assess effects on differentiation markers Determine causal
link between reduced proliferation and accelerated maturation

3. Rescue experiments Verify specificity by restoring proliferation in otherwise differentiated cells Reintroduce Cyclin D1 after initial inhibition; monitor
whether maturation stalls or reverses Confirm that proliferation is
necessary for maturation to proceed

4. Long‑term functional assays Evaluate whether altered
proliferation impacts electrophysiology and synaptic integration Patch‑clamp
recordings, calcium imaging, connectivity mapping Ensure that acceleration of
maturation does not compromise function

Through these systematic perturbations—temporal reduction of cell cycle activity followed by restoration or blockade—and detailed phenotypic readouts (proliferation markers, differentiation stages, functional assays),
one can determine whether the observed correlations between proliferation and neuronal maturation are
causal. The design explicitly tests for necessity (by blocking proliferation) and sufficiency (by accelerating it), while controlling for confounding factors such
as cell density or microenvironment changes. This approach aligns with the article’s emphasis on understanding how dynamic cellular behaviors
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Anavar, also known by its chemical name oxandrolone, is a
synthetic anabolic steroid that has gained popularity among athletes
and bodybuilders for its ability to promote lean muscle mass while minimizing water retention. When combined with testosterone in a cycle, users aim to harness the complementary effects of both compounds:
testosterone provides the foundational anabolic stimulus necessary for overall strength and recovery, whereas Anavar offers a more subtle but efficient pathway for building hard,
defined musculature without excessive bulk or edema. A typical cycle that blends these two agents
often spans eight to twelve weeks, with careful attention paid to dosage,
timing, and post‑cycle therapy (PCT) to mitigate potential side effects.

Test and Anavar Cycle

The classic approach begins with a baseline of
testosterone, usually administered via intramuscular injection or subcutaneous implant.
A common dosage is 200 mg per week for men, though advanced users sometimes
increase this to 250–300 mg per week depending on their tolerance
and training goals. The testosterone component should be started at least
two weeks before introducing Anavar, allowing the body to stabilize hormone levels and
reduce the risk of sudden hormonal fluctuations.

Oxandrolone is introduced around week three or four of the cycle.
Dosages for Anavar typically range from 20 mg to 40 mg per day for
men, with women generally prescribed half that amount due to heightened
sensitivity. The daily administration schedule can be split into two equal doses (morning and evening)
to maintain steadier blood levels. Over the course of
the cycle, users may gradually increase Anavar dosage if tolerated, but it is advisable to keep within the 30–40 mg
per day range to avoid liver strain.

Throughout the eight‑to‑twelve week period, careful monitoring of testosterone levels
through blood panels every two weeks can help fine‑tune dosages.
Hormone ratios are also monitored to ensure that the anabolic drive from testosterone does not overwhelm the body’s natural equilibrium.

This balanced approach minimizes risks such as gynecomastia, acne, or mood disturbances.

At the end of the cycle, a structured PCT is essential.
The goal is to restore endogenous testosterone production and protect the liver from potential cumulative damage.
Common agents used in PCT include selective estrogen receptor modulators (SERMs) like clomiphene citrate or tamoxifen, as well as aromatase inhibitors if estrogen levels rise.
A typical 4‑week PCT might involve clomiphene at 25 mg per
day for the first two weeks, followed by a tapering
schedule in the third week and cessation in the fourth.

What is Testosterone?

Testosterone is a steroid hormone produced primarily in the
Leydig cells of the testes in men, with smaller amounts generated
in the adrenal glands. It plays a pivotal role in developing male
secondary sexual characteristics, such as facial hair growth, deepening
of the voice, and increased muscle mass. Beyond these physical traits, testosterone contributes significantly to
mood regulation, libido, energy levels, and overall sense of well‑being.

From an anabolic perspective, testosterone promotes protein synthesis by stimulating ribosomal activity within cells, which
leads to faster repair of muscle fibers after intense training sessions.
It also enhances nitrogen retention in the muscles, a
key factor for sustaining growth over time.
In addition, testosterone can boost erythropoiesis (red blood
cell production), thereby improving oxygen delivery to working tissues and supporting endurance performance.

Because of its powerful effects on both muscular development and recovery, testosterone is often used as
the cornerstone of anabolic steroid cycles.
When combined with a milder agent like Anavar, it
provides a synergistic effect: testosterone delivers robust anabolic energy while Anavar refines muscle definition without causing
excessive water retention or fat gain.

Key Takeaways

Combining testosterone with Anavar in an eight‑to‑twelve week cycle can produce significant lean muscle gains while limiting unwanted side effects such as bloating and gynecomastia.

A typical regimen involves starting testosterone at 200–300 mg per week,
then adding Anavar at 20–40 mg daily after the first few weeks of stabilization.

Regular blood panels every two weeks are recommended to monitor
hormone levels, liver enzymes, and overall health markers throughout
the cycle.

Post‑cycle therapy with SERMs or aromatase inhibitors is critical for restoring natural testosterone production and preventing estrogen‑related complications.

Understanding the distinct roles of each compound—testosterone as a powerful anabolic base and Anavar as a lean muscle enhancer—helps users design safer, more effective training protocols.

By carefully balancing dosage, timing, and monitoring, individuals
who incorporate both testosterone and Anavar into their training regimen can achieve a pronounced increase
in strength, muscularity, and overall athletic performance while
minimizing the risk of adverse health outcomes.