#Protein Targeting

[mavisgarygotsober]

Target was having some kind of clearance in their protein bar section. I got 2 packs of Alani protein bars, a target brand of bars, and 5 energy drinks for like $22. I’m not mad at any of that

[artisanalpeanutbutter]

Trying to build muscle is so frustrating bc it's hard enough to motivate myself to eat as it is but now I have to eat more protein and my stomach is too liddol for the amount of food I need in a day

Can I get an f in the chat?

[whats-in-a-sentence]

You are an organized bundle of refined energy, essential elements, and machinery for making proteins: an irresistible target.⁹

9. Parasites (except viruses) must acquire both energy and required elements. We would do well not to underestimate the twenty-five elements required for life as a limiting factor on genetic success; free iron, for instance, is a critical and scarce biological resource, and hosts and parasites tussle over it.

"Plagues Upon the Earth: Disease and the Course of Human History" - Kyle Harper

[blueoaknx]

Mitochondrial Dysfunction in Spinal Muscular Atrophy (SMA)

Introduction

Spinal Muscular Atrophy (SMA) is a severe neurodegenerative disorder that predominantly affects motor neurons, resulting in progressive muscle weakness and atrophy. The condition is caused by mutations in the survival motor neuron 1 (SMN1) gene, which leads to the loss of SMN protein, a critical factor for motor neuron survival. Although the primary defect lies in the motor neurons, increasing evidence suggests that mitochondrial dysfunction plays a pivotal role in the pathophysiology of SMA. Mitochondria, the powerhouse of the cell, are crucial for cellular energy production and regulation of various metabolic pathways. In the context of SMA, mitochondrial dysfunction has been linked to impaired cellular energy metabolism, oxidative stress, and neuronal death.

This article reviews the emerging role of mitochondrial dysfunction in SMA, examining its impact on motor neurons, the cellular processes involved, and the potential for mitochondrial-targeted therapies.

Mitochondrial Dysfunction in SMA: A Pathophysiological Overview

Mitochondria are essential organelles responsible for generating ATP through oxidative phosphorylation, controlling cellular metabolism, and mediating cell death mechanisms. In SMA, deficits in SMN protein affect multiple cellular pathways, including mitochondrial function. SMN is known to be involved in the biogenesis and maintenance of mitochondria. When its expression is reduced, mitochondrial dysfunction occurs in several ways, contributing to the progressive nature of SMA.

Impaired Mitochondrial Biogenesis

Mitochondrial biogenesis refers to the process by which new mitochondria are formed within cells. This process is tightly regulated by nuclear and mitochondrial signals, with the peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) being a key regulator of mitochondrial biogenesis. Studies in SMA models have shown that a reduction in SMN protein leads to downregulation of PGC-1α, resulting in decreased mitochondrial biogenesis. This reduced mitochondrial mass is particularly detrimental to motor neurons, which have high energy demands due to their long axonal projections and rapid neurotransmitter signaling.

Mitochondrial Dysfunction and ATP Production

Mitochondrial dysfunction in SMA results in decreased ATP production. ATP is required for essential cellular functions such as protein synthesis, ion transport, and maintaining membrane potential. In motor neurons, impaired ATP generation leads to cellular energy deficits that exacerbate neurodegeneration. Mitochondrial dysfunction also disrupts calcium homeostasis, as mitochondria play a central role in buffering intracellular calcium levels. Elevated intracellular calcium levels can activate enzymes that degrade cellular components, further contributing to cell death in motor neurons.

Oxidative Stress

One of the most significant consequences of mitochondrial dysfunction is the increased production of reactive oxygen species (ROS). Mitochondria are the main source of ROS in cells, and under normal conditions, the antioxidant defense systems neutralize these reactive molecules. However, in SMA, defective mitochondrial function leads to excessive ROS production, which overwhelms the cell’s ability to detoxify them. ROS are highly reactive and can damage cellular structures such as proteins, lipids, and DNA, ultimately contributing to oxidative stress and neuronal injury.

Mitochondrial Dynamics and Morphology

Mitochondrial morphology is highly dynamic, with the organelles undergoing fusion and fission events in response to cellular needs. In SMA, the balance between these processes is disrupted. Studies have shown that reduced SMN levels lead to an increase in mitochondrial fragmentation, a characteristic of mitochondrial dysfunction. Fragmented mitochondria are less efficient in energy production and more prone to damage. Additionally, the fragmented mitochondria in SMA models exhibit impaired mitochondrial transport along axons, further hindering motor neuron function.

Mitochondrial Quality Control

Mitochondrial quality control mechanisms, such as mitophagy, are critical for maintaining mitochondrial health. Mitophagy is the process by which damaged mitochondria are selectively degraded by autophagosomes. In SMA, defects in SMN protein affect the cellular machinery responsible for mitophagy, leading to the accumulation of dysfunctional mitochondria. This impairment in mitochondrial turnover accelerates neurodegeneration by allowing damaged mitochondria to persist, increasing oxidative stress, and triggering cellular apoptosis.

Mitochondrial Dysfunction in Different Types of SMA

SMA is classified into several types based on age of onset and severity, including Type I (Werdnig-Hoffmann disease), Type II, Type III, and Type IV. Mitochondrial dysfunction is observed in all types, but its extent varies depending on the severity of the disease.

SMA Type I

This is the most severe form of SMA, typically presenting in infants before six months of age. These children experience profound muscle weakness and may not survive beyond the first two years of life without intervention. In Type I, mitochondrial dysfunction is particularly pronounced, with severe mitochondrial fragmentation, impaired ATP production, and significant oxidative damage observed in motor neurons. The severity of mitochondrial dysfunction correlates with the extent of neurodegeneration in the spinal cord.

SMA Type II

Type II SMA presents later in infancy or early childhood, with affected individuals showing progressive muscle weakness but with a longer life expectancy compared to Type I. Mitochondrial dysfunction in Type II is still significant but less severe than in Type I. There is evidence of mitochondrial fragmentation and altered mitochondrial dynamics, but motor neurons in Type II patients may still retain some capacity for mitochondrial biogenesis and ATP production, contributing to the slower progression of the disease.

SMA Type III and IV

SMA Type III and IV are milder forms of the disease, with onset typically in childhood or adulthood. While mitochondrial dysfunction is present, it is less pronounced than in Type I and II. In these types, mitochondrial dynamics, ATP production, and oxidative stress are affected, but the clinical presentation is less severe, and individuals often experience a normal or near-normal life expectancy.

Conclusion

Mitochondrial dysfunction is a central feature of the pathophysiology of Spinal Muscular Atrophy (SMA). Reduced SMN protein leads to impaired mitochondrial biogenesis, altered mitochondrial dynamics, increased oxidative stress, and mitochondrial dysfunction. These defects contribute to the progressive degeneration of motor neurons and muscle weakness seen in SMA. Understanding the complex interplay between SMN deficiency and mitochondrial dysfunction provides valuable insights into the disease mechanisms and offers new avenues for therapeutic intervention. Mitochondrial-targeted approaches, including enhancing mitochondrial biogenesis, antioxidant therapy, and modulation of mitochondrial dynamics, hold promise for improving the quality of life and outcomes for SMA patients.

Ongoing research into mitochondrial dysfunction in SMA is crucial for identifying novel treatment strategies that can complement existing therapies and slow disease progression. As therapeutic options evolve, mitochondrial health will likely become an important consideration in the management of SMA, offering hope for more effective treatments in the future.

[bluepoodle7]

#Target#TargetGoodAndGatherProteinPackTurkeySausageAndColbyJackCheeseQuickBites#TurkeySausageAndCheeseSnack#SnackKitsReview

This is part 2 of the Target Good And Gather Protein Pack Turkey Sausage And Colby Jack Cheese Quick Bites.

These are the rest of the images.

Part 1

#Target#TargetGoodAndGatherProteinPackTurkeySausageAndColbyJackCheeseQuickBites#TurkeySausageAndCheeseSnack#SnackKitsReview These... – @bluepoodle7 on Tumblr

[dyna-myght]

Trying to tell my dad about how my diet is going and how I think it’s something super sustainable for me in the long term bc it’s just pre portioned dinners that take 15 minutes to cook. And his fucking response was to like suggest other different diets I can do. Like can he just be supportive for once…. Especially bc my diet is almost exactly what his own doctor prescribed him anywaysssssss. Plus I don’t trust him bc. Last time he was doing a carnivore diet before his body started to go haywire because of it.

[mysticalpeacenut]

Advancements in PPI Targeted Drug Discovery

In the ever-evolving international of drug discovery, concentrated on protein-protein interactions (PPIs) has emerged as a groundbreaking method with massive healing capacity. While traditional drug discovery has largely focused on focused on single proteins or enzymes, the point of interest is shifting toward the intricate networks fashioned by using protein interactions. These networks are critical to expertise disorder mechanisms and growing innovative treatments. This blog delves into the modern day advancements in PPI targeted drug discovery, highlighting the transformative impact of Protein-Protein Interactions Magna™ technology and different modern tactics.

Understanding Protein-Protein Interactions

Protein-protein interactions are essential to almost each biological manner. Proteins not often function in isolation; as a substitute, they interact with different proteins to carry out their functions. These interactions can manipulate cell signaling pathways, adjust gene expression, and influence cell responses to environmental changes. Disruptions or malfunctions in those interactions are frequently implicated in diseases which include cancer, neurodegenerative problems, and infectious diseases.

PPI Targeted Drug Discovery makes a speciality of designing drugs which could especially modulate these protein interactions. Unlike conventional capsules that focus on a single protein, PPI-centered pills purpose to persuade the interactions among multiple proteins, thereby imparting a greater nuanced approach to therapeutic intervention.

Key Advancements in PPI Targeted Drug Discovery

Protein-Protein Interactions Magna™ Technology

One of the maximum giant advancements in PPI-focused drug discovery is the development of Protein-Protein Interactions Magna™ technology via Depixus. This modern day era gives a complete platform for analyzing and manipulating protein interactions with remarkable precision.

Magna™ generation uses advanced techniques to seize and examine how proteins engage within a cellular surroundings. By offering special insights into these interactions, Magna™ permits researchers to become aware of ability drug goals and design molecules that may in particular disrupt or decorate those interactions. This method is vital for growing healing procedures that focus on complicated sicknesses wherein conventional drug discovery methods may additionally fall brief.

High-Throughput Screening

High-throughput screening (HTS) has revolutionized PPI-centered drug discovery via permitting the rapid evaluation of lots of compounds for their capability to modulate protein interactions. HTS structures use automated structures to test big libraries of molecules against particular PPIs, identifying promising applicants for further development.

Recent improvements in HTS technology have expanded the speed and accuracy of screening processes. Innovations consisting of miniaturized assays, stepped forward detection techniques, and sophisticated statistics analysis gear have substantially better the efficiency of PPI-targeted drug discovery.

Structural Biology Techniques

Structural biology strategies, together with X-ray crystallography, nuclear magnetic resonance (NMR) spectroscopy, and cryo-electron microscopy, have supplied vital insights into the three-dimensional structures of protein complexes. Understanding the ideal structure of protein-protein interactions is essential for designing drugs which could in particular goal those interactions.

Recent traits in structural biology have enabled researchers to visualize protein interactions at atomic resolution, facilitating the design of small molecules and biologics which could efficiently disrupt or stabilize those interactions. This structural records is invaluable for growing centered treatment options with high specificity and decreased off-goal outcomes.

Computational Approaches

Computational methods, which includes molecular docking and molecular dynamics simulations, have end up necessary gear in PPI-targeted drug discovery. These techniques use pc algorithms to predict how small molecules or peptides will interact with protein complexes, guiding the layout of recent drugs.

Advancements in computational techniques have improved the accuracy of predictions and the efficiency of digital screening techniques. By simulating protein interactions and drug binding, researchers can pick out ability drug applicants and optimize their homes earlier than conducting experimental research.

Biologics and Peptide-Based Therapies

Biologics, along with monoclonal antibodies and peptide-based totally remedies, constitute a growing vicinity of hobby in PPI-focused drug discovery. These cures are designed to specially bind to protein interactions and modulate their activity.

Recent advancements in biologics and peptide design have caused the development of novel drugs that concentrate on PPIs with excessive specificity. For instance, bispecific antibodies which could simultaneously bind to two exclusive proteins are being explored as potential cures for numerous sicknesses.

The Future of PPI Targeted Drug Discovery

The subject of PPI focused drug discovery is swiftly advancing, with ongoing research aimed toward overcoming current challenges and increasing the range of druggable objectives. The integration of new technology, which includes Protein-Protein Interactions Magna™, structural biology, excessive-throughput screening, and computational strategies, is riding innovation and opening up new possibilities for therapeutic intervention.

As researchers hold to explore the complexities of protein interactions, the capability for growing novel treatments that concentrate on previously undruggable sicknesses grows. The capability to especially modulate protein-protein interactions offers a brand new stage of precision in drug development, paving the way for extra effective and focused remedies.

Conclusion

PPI focused drug discovery represents a paradigm shift in how we technique drug development, shifting beyond traditional single-protein objectives to focus on the tricky networks of protein interactions. With advancements which include Protein-Protein Interactions Magna™ era and other present day tactics, the sector is poised for great breakthroughs so one can remodel the landscape of medicine. At Depixus, we're at the leading edge of this thrilling field, providing innovative solutions and technologies that aid researchers of their quest to broaden the next generation of centered healing procedures. To study extra approximately how our Protein-Protein Interactions Magna™ generation can decorate your research and pressure innovation contact us at Depixus.

Reposted Blog Post URL: https://petrickzagblogger.wordpress.com/2024/09/04/advancements-in-ppi-targeted-drug-discovery/

[girlwithrituals]

GLOW UP GUIDE FOR 2025⠀

READ: On average, it takes more than 2 months before a new behavior becomes automatic — 66 days to be exact. And considering that 2025 is precisely these many days away, why not start with our glow up plan already?

Physical Glow Up-

BODY

— 5-10K steps a day.

— 7-8 hours of sleep.

— workout everyday for 1 hr atleast- yoga/stretching/pilates/cardio/lifting weights. a workout may take one hour, but your mood will be boosted for the next 12 hours.

— posture training.

— sunlight exposure after waking up for at least 10 minutes.

NUTRITION

— 2-3 liters of water every day.

— limit your caffeine intake.

— avoid sugars as much as you can.

— high protein diet, pre and probiotics.

— more fruits and veggies (+ green smoothies if you like).

— no junk/processed food/trans fat.

— no eating after 8 pm.

SKINCARE

— be clear on your skin type (oily, dry, combination, sensitive).

— once you're clear, use these accordingly- cleanser, toner, targeted serum, eye cream, moisturizer, sunscreen (≥50 spf).

— keep your bedding clean as well.

— no picking of skin on your lips, cuticle etc.

— gua sha to help improve blood circulation and lessen toxins.

— cold therapy may take three to five minutes of being uncomfortable, but your energy levels will be boosted for the rest of the day.

— remove makeup before you go to bed.

BODY CARE

— shower every day.

— exfoliate 2x a week.

— use body lotion (shea butter/aloe vera gel/coconut oil).

HAIR CARE

— wash hair 2-3x a week

— oil your scalp 2x a week, at least 3 hours before shampoo.

— hair mask 1x per week.

— never brush wet hair.

— use silk pillow case.

HYGIENE

— brush your teeth 2x a day, clean tongue and the roof of the mouth daily.

— floss daily.

— cut your nails 1x a week, never remove the cuticles.

— glycolic acid under arm for odor and discoloration.

— never use soap on your coochie.

Mental Glow Up-

MINDSET

— set clear goals- define and breakdown your aspirations.

— start your mornings with positive affirmations.

— surround yourself with uplifting content and people.

— be shamelessly selfish to your career and mental health, remove anyone or anything that doesn't align with your priorities and wellbeing.

— boost your brain health by these 4 neuroscience tools:

difficult first: start your day with the most difficult task (cortisol and dopamine are high in the body meaning that your body/mind is primed to work).

rest your eyes: introduce a micro-pause after learning by resting/closing your eyes - will help retain information better.

tomorrow's worries: write tomorrow's to-do list before bed as it is proven to be effective in helping you fall asleep.

find time to play: engage in low-stake play. can be anything you find fun but where the outcome doesn't matter (induces neuroplasticity + reduces stress).

MIND

— meditation might take as low as ten minutes, but your focus will be improved for the rest of the day.

— no social media after waking up and at least an hour before bed.

— keep aside 1 hr of time to read daily! reading a new book may take five hours, but you will keep the knowledge forever.

— journaling, gratitude.

— digital detox once a week or for 12 hours.

— limit unnecessary screentime, unfollow or cut off people you don't want to see.

JOURNALING

— choose a regular time each day to journal, making it a part of your routine.

— find a quiet, comfortable place free from distractions. light a candle if you want.

— allow your thoughts to flow without censoring or editing.

— write about your feelings and emotions to understand them better. write about things you are thankful for to boost your mood. write about your short-term and long-term goals. identify what triggers certain emotions or reactions

— set a timer for 5-10 minutes and write continuously during that time.

— reflect on both positive experiences and challenges.

— make lists, journal your thoughts on these questions.

— journal at night to clear your mind before bedtime, because emotions and thoughts lose their power once we acknowledge them.

— a gratitude practice may take five minutes, but your mindset will be shifted for the rest of the day.

AFFIRMATIONS

— customise affirmations to your needs.

Personal Life-

WEEKLY TASKS

— initiate small changes: begin with small, manageable tasks such as making your bed or cleaning your room every sunday.

— celebrate your success: reward yourself when you achieve your goals or have a consistently productive week. consider treats like buying flowers for yourself or watching your favorite show.

DAILY WORK

— set achievable goals: establish realistic goals for the day, week, or month ahead.

— track your progress.

— organise your work space, declutter your shelves etc.

— embrace the power of lists: keep a list of tasks to be done and their deadlines. this way, you start each day with a clear plan. to make it visually appealing and motivating, consider using productivity apps like evernote, habit tracker, or notion.

PRODUCTIVITY TIPS

— wake up early.

— plan ahead everything, do scheduling. you can use:

google calendar / notion / tasks .

— if the task takes less than 2 minutes to finish, do it immediately.

— countdown rule, if you are procrastinating, count 1-2-3-4-5 and jump.

— start slow, don't rush and try to do everything at one time.

— follow a proper routine, use app locks based on screentime.

— pomodoro technique, 25 min work, and 5 min break.

— schedule longer break times as well e.g 30 min nap.

[reasonsforhope]

"A medical technology company in Australia is aiming for a world-first: it wants to launch a blood test for endometriosis (sometimes called 'endo' for short) within the first half of this year [2025].

In a recent peer-reviewed trial, its novel test proved 99.7 percent accurate at distinguishing severe cases of endometriosis from patients without the disease but with similar symptoms.

Even in the early stages of the disease, when blood markers may be harder to pick out, the test's accuracy remained over 85 percent.

The company behind the patent, Proteomics International, says it is currently adapting the method "for use in a clinical environment," with a target launch date in Australia for the second quarter of this year [2025].

The test is called PromarkerEndo.

"This advancement marks a significant step toward non-invasive, personalized care for a condition that has long been underserved by current medical approaches," managing director of Proteomics International Richard Lipscombe said in a press release from December 30.

Endometriosis is a common inflammatory disease that occurs when tissue similar to the lining of the uterus grows in other parts of the body, forming lesions. The disease can be very painful, and yet the average patient often suffers debilitating symptoms for up to seven years before they are properly diagnosed.

While there are numerous reasons for such a long delay, symptoms of endometriosis are often highly variable, unpredictable, difficult to measure or describe, and dismissed or overlooked by doctors.

Today, the only definitive way to diagnose endometriosis is via keyhole surgery called a laparoscopy, which is expensive, invasive, and carries risks.

Proteomics International is hoping to change that.

In collaboration with researchers at the University of Melbourne and the Royal Women's Hospital, the company compared the bloodwork data from 749 participants of mostly European descent.

Some had endometriosis and others had symptoms that were similar to endo but without the lesions. All participants had a laparoscopy to confirm the presence or absence of the disease.

Sifting through the bloodwork, researchers ran several different algorithms to figure out which proteins in the blood were best at predicting endometriosis of varying stages.

Building on previous research, a panel of 10 proteins showed a "clear association" with endometriosis.

For years now, scientists have investigated possible blood biomarkers of endometriosis to see if they could differentiate between those who have endo and those who do not. Similar to cancerous tumors, endo lesions can establish their own blood supply, and if cervical cancer can be diagnosed via a blood test, it seemed possible that endometriosis could be, too...

Proteomics International claims patents for PromarkerEndo are "pending in all major jurisdictions," starting first in Australia.

It remains to be seen if the company's blood test lives up to the hype and is approved by the Australian Therapeutic Goods Administration (TGA). But that's not outside the realm of possibility.

In November of 2023, some researchers predicted that a "reliable non-invasive biomarker for endometriosis is highly likely in the coming years."

Perhaps this is the year."

-via ScienceAlert, January 9, 2025

--

Note: As someone with endometriosis, let me say that this is a HUGE deal. The condition is incredibly common, incredibly understudied, and incredibly often dismissed. Massive sexism at work here.

I got very lucky and got diagnosed after about 6 months of chronic pain (and extra extra lucky, because my pain went away with medication). But as the article says, the average time to diagnosis is seven years.

Being able to confirm endometriosis diagnoses/rates without invasive surgery will also lead to huge progress in studying/creating treatments for endo.

And fyi: If you have a period that is so painful that you can't stand up, or have to go home from school/work, or vomit, or anything else debilitating (or if any of those things apply if you forget to take pain meds), that is NOT NORMAL, and you should talk to a competent gynecologist asap.

[buckysleftbicep]

cradles and chaos 𐙚 b.b

pairing: new avenger!bucky barnes x pregnant!fem!reader

warning: morning sickness, loads of fluff, and team shenanigans

summary: you wanted to surprise bucky with the news—you’re pregnant. the only problem? everyone else on the team found out first. cue the chaos.

word count: 3.5k

author's note: i love writing fics with teeth rotting fluff, genuinely love them so much! i hope you enjoy them, i love ya and stay safe out there!

requests are open! i love, love, love soft!bucky

The day started like any other.

Morning training. Groggy coffee run. Bucky kissing the top of your head before heading off to spar with Alexei and you trying not to gag at the smell of the protein powder he insisted on putting in his smoothie. Just the usual.

Until it hit you.

The wave of nausea crashed into your gut so suddenly that you barely made it to the compound bathroom in time. Knees on the cold tile, you gripped the toilet bowl and dry-heaved like you were trying to launch a demon from your oesophagus.

It was violent. Loud. And, unfortunately for you, not private.

Footsteps approached behind you, followed by a dry, unimpressed voice. “If this is your version of The Exorcist, you forgot the head spin. Come on, at least commit to the bit.”

You groaned. “Yelena, for the love of—”

She stepped inside without hesitation, casually grabbing a hair tie from her wrist and gathering your hair like this was a weekly occurrence. “Let me guess. Either Alexei made you try his ‘secret stamina shake’ again, or…” Her eyes narrowed. “You’re pregnant.”

Your blood ran cold.

“Wait,” she said, pausing mid-sentence. Her expression changed, slowly morphing into that wide-eyed look she got when she spotted a new target. “Wait. Wait.”

“Don’t—”

“YOU’RE PREGNANT.”

“Shhh!” You jumped up and flushed the toilet like it would somehow erase the moment. “Keep it down!”

Yelena’s face lit up like a Christmas tree. “You are! Oh my god. I knew it. That explains the pickles and peanut butter at two in the morning. Also, the weird crying over that dog food commercial last week.”

“I was hormonal! That golden retriever had abandonment issues!”

“I’m not judging,” she said, clearly enjoying this too much. “I’m just honoured to be the first to know. Or like, second, I guess?”

You bit your lip. “…He doesn’t know yet, does he?”

She froze. “Wait. You haven’t told Bucky yet?”

You winced. “Not yet. I wanted to surprise him. Big surprise. Sweet. Emotional. Crying, maybe him, not me. I’ve cried enough.”

Yelena blinked twice. Then her hand flew to her chest in dramatic horror. “Oh my God. I am in charge of a secret. I’m responsible for withholding information from Barnes. Do you know what this means?”

“That I trust you?”

“That I’m going to be the best fucking godmother in the world.”

You finally breathed again, until she added, “Though… I am tempted to tell the others."

“Yelena.”

“Relax,” she said with a shrug. “Your secret’s safe. For now. But if you die, I get to raise the kid like a tiny assassin. Deal?”

“…Yelena.”

“Deal?”

“…Fine.”

She grinned, already scheming.

You had taken every precaution.

No more sparring. No caffeine. Your prenatal vitamins were hidden behind a bag of trail mix no one ever touched. You kept your hoodie on at all times, avoided combat drills, smiled through nausea, and faked normalcy like your life depended on it.

But Ava wasn’t the type to be fooled by quiet exits and thicker sweatshirts.

She didn’t ask questions. She didn’t need to. She just watched. The way a blade waits in the dark, calculating without moving. You could feel it—her eyes on you during training, her steps falling in line behind yours a little more often than before.

One morning, you reached for your weighted vest only to find it mysteriously lighter. Five pounds missing. No explanation. She said nothing.

Then one night in the rec room, you were curled up on the couch half-watching some movie you’d already forgotten the plot of, when a packet of ginger chews landed softly in your lap. You looked up, startled.

Ava didn’t turn. She was sitting in the armchair across the room, casually typing something on her tablet like she hadn’t just sniped you with snacks.

“You gagged in the elevator this morning,” she said, still not looking at you. “Second time this week.”

You blinked, fingers tightening around the ginger chews. “I—maybe I’m just coming down with something.”

She didn’t answer. Just gave the softest hum. Like she was humoring you. You waited for her to press, to demand answers, to ask what Bucky somehow hadn’t noticed yet.

But she didn’t.

“You’re not gonna say anything?” you asked after a beat, quieter now.

“I don’t care,” she said, voice flat, eyes on her screen. “Unless you get yourself killed. Then it becomes my problem.”

You exhaled through your nose, smiling despite yourself. “So this is you being… concerned?”

“This is me avoiding paperwork.”

You bit your lip to stop yourself from laughing. Ava didn’t do affection, not in the traditional sense. She did proximity. Action. Silence that somehow felt like reassurance. She didn’t say much, but she never missed anything.

“Don’t carry anything heavy,” she added after a moment, her tone just as even, like she was reading off a grocery list.

Over the next week, you noticed the little things.

A decaf coffee cup on your desk, slid across the surface wordlessly while she passed by. Her cutting her own training short to spot you during stretches, silent and watchful, and you were never more grateful.

Once, you opened your locker and found a small bottle of prenatal vitamins tucked neatly beside your usual supplements. The label had been peeled off. There was no note. But you knew exactly where they came from.

Bucky, meanwhile, remained adorably clueless.

He still kissed your cheek every morning, still asked if you wanted spicy noodles, the ramen kind for dinner, still rubbed your back when you sighed too hard without even realising why you were sighing.

“You’ve seemed kinda tired lately,” he said one night, brushing a strand of hair from your face. “You okay?”

And just like that, Bucky let it go.

The next morning, there was a new water bottle waiting on your desk. One of those fancy ones with the hours marked on the side like hydration was a full-time job. You didn’t need to guess who left it there.

Ava just knew. And that was enough.

It was bound to happen.

You were doing your best. Truly. Between Yelena’s feral excitement and Ava’s silent protection, you were managing.

Bucky was still clueless (somehow), not that you were complaining, and the rest of the team had stayed suspiciously uninvolved.

But then came Alexei.

Loud, dramatic, built like a brick wall and absolutely no understanding of what the word subtle meant.

You didn’t mean for him to find out. In fact, you weren’t even in the room when it happened.

It started in the kitchen.

You’d left your tea steeping on the counter—ginger with a splash of lemon, the only thing that didn’t make you want to retch—and stepped out to grab your hoodie from the lounge.

Two minutes. Maybe less.

And that’s when disaster struck.

Alexei strolled in, whistling some vaguely patriotic tune, spotted the mug, and immediately sniffed it like a bloodhound. You weren’t even there to defend yourself.

“Hm,” he muttered to himself. “This tea… I know this tea. My babushka (russian for grandmother) used to make this for woman in village. When they were… what’s word? With child.”

From across the kitchen island, Yelena looked up from her cereal with mild panic in her eyes.

“Do not do this,” she warned, spoon halfway to her mouth.

Alexei didn’t listen.

Instead, he sniffed the tea again, leaned back with both hands on his hips like some kind of Soviet sommelier, and declared, “It is pregnancy tea! Very good for nausea. Calms stomach. Boosts circulation. Ancient remedy.”

Yelena slowly set her spoon down. “Alexei—”

“WAIT.” His eyes widened. “IS SHE WITH CHILD?!”

You walked in just in time to see him throw both hands into the air and look around like he expected confetti to fall from the ceiling. “IS THERE A BABY? ARE WE HAVING BABY?!”

Yelena let her head thunk against the table. “You absolute moron.”

Alexei turned to her with wild-eyed enthusiasm. “YOU KNOW?!”

“Of course I knew, you donkey. Bucky doesn't, yet."

He gasped like someone had stabbed him—but dramatically, like an actor in a very bad stage play. “You betray me! I am her family. I am her protector. I am baby future grandfather!”

“I’m gonna throw up,” Yelena muttered.

And then he saw you.

Alexei’s expression softened, somehow, impossibly, turning from full-volume chaos to absolute, genuine awe. He crossed the room in two heavy strides, grabbed your hands in his like you were made of glass, and stared at you like you were the eighth wonder of the world.

“You,” he said, lowering his voice like it physically hurt him to be gentle, “are miracle.”

“Okay—”

“No, listen. You are tiny, like small baby rabbit, but you carry powerful legacy. You carry strength. Heart. Warrior blood."

Alexei cupped your face—not quite gently, but at least without crushing your skull—and nodded to himself like he was solving a world crisis. “I will protect this child with everything I have. I will teach them discipline. Honour. How to disarm man in six seconds. Also fishing.”

“Alexei—”

“Shhh.” He tapped your forehead. “Little Starfish, you are busy now. You grow hero. I will build cradle. I have plans already. And foam. And tools. Maybe missile too.”

You stared at him.

“…Please don’t put missiles near the baby.”

“Decorative.”

Yelena snorted.

Alexei turned back to her. “We need banner. And possibly anthem. Something that plays when child enters room.”

You sighed into your palm. “No one is making an anthem for the baby.”

He placed a hand over his chest. “We see.”

You didn’t mean to drag John into it. Not directly, anyway.

But desperate times called for desperate measures.

You were curled up on the compound couch one afternoon, hoodie pulled over your knees, watching a rerun of Shark Tank and trying your absolute best not to commit murder out of pure hormonal rage when the craving hit, hard, out of nowhere.

You held out for a few minutes—tried breathing, counting backwards, chewing on the inside of your cheek. But by minute five, your resolve crumbled. You pulled out your phone and fired off a text.

you up? can you get me mango gummies. and pickles and vanilla yogurt. not greek. please.

There was a pause. Then:

Walker: you want me to bring you pickles and yogurt?

You: together. in the same container. i'm gonna dip them.

Another pause. Longer.

Walker: that's weird, but I’m on my way.

True to his word, John showed up twenty minutes later, slightly out of breath like he had sprinted through a Costco. He had two grocery bags in hand and a look on his face that said he had seen war—but nothing quite like this.

“Okay,” he said, dropping the bags like they might detonate, “I got four kinds of yogurt because I didn’t know what you meant, three kinds of pickles because apparently there are options, and the mango gummies."

You blinked, mildly overwhelmed. “You're a hero."

He didn’t move. Just stood there, watching as you cracked open the yogurt, dunked a pickle, and took a bite like it was the most normal thing in the world. You let out a blissed-out sigh.

John stared, horrified. “You’re really eating that?"

“Yup.”

“Like... voluntarily?”

“It’s good.”

He sat down beside you slowly, arms crossed like a disappointed gym teacher. “I don’t think that’s how taste buds work.”

You shrugged, popping another pickle. “Maybe not for you.”

There was a long silence. Then John tilted his head back, staring at the ceiling like it held answers. “Okay,” he muttered. “You cried during that dog adoption video last week.”

“So did you,” you pointed out.

“Yeah, but you sobbed. Like, full on ugly cry. For twenty minutes. Over a golden retriever named Meatball.”

“He was alone in the shelter for six years.”

“And then there’s the naps. The weird tea. The fact that Ava’s been hovering. And now you’re eating that.” He gestured vaguely at your snack combo, then narrowed his eyes.

“Wait. You sparred with me the other day and said my voice gave you a headache.”

You didn’t even look up. “Sometimes it does.”

His eyes went wide. “Oh my God. You’re pregnant.”

You froze, mid-bite.

He gasped and stood up so fast the couch groaned. “You’re pregnant, and I gave you a concussion last month!”

“I was already pregnant,” you said flatly. “You just didn’t know it.”

“Oh my God.” He started pacing, one hand on his head. “I told you to lift heavier weights. I told you to jump off that ledge. You had two plates of nachos for breakfast last week and I mocked you.”

“John—”

“I called you a sleepy turtle.”

“John,"

He turned, wild-eyed. “Am I complicit?”

You blinked. “In the pregnancy?”

He looked genuinely uncertain. You let out a long breath. “No, John. You are not.”

There was a pause. A beat of silence. Then he nodded once and walked to the kitchen like a man on a mission. A minute later, he returned with a glass of orange juice and handed it to you like it was a peace offering from a defeated warrior.

After that, he slumped onto the couch beside you with a dramatic sigh, arms flopping out over the cushions.

“I’m gonna be such a bad uncle,” he muttered.

You nudged him gently with your shoulder. “You’ll be fine.”

“I brought four kinds of yogurt.”

You smiled. “You’ll be great.”

Bob found out by accident.

You were in the mess hall, quietly sipping ginger tea and trying not to vomit over the smell of John’s overly seasoned reheated chili, when Bob slid into the seat across from you with a smile and a soft, “Hey.”

“Hey,” you managed.

He blinked at the tea. Then at the saltines. Then at the way you were ever-so-subtly glaring at the chili across the room like it had personally wronged you.

“You okay?”

“Yeah,” you said too fast. “Fine. Just a headache.”

Bob’s brows pinched together. He looked concerned. Thoughtful. And then, as if connecting puzzle pieces like the others had in real time, tilted his head. “Wait. Is this… like a headache-headache or a pregnant and trying not to barf from chili fumes headache?”

You froze.

His eyes widened. “Oh my god. Oh my god. Are you—?”

You sighed, smiling sheepishly. “You weren’t supposed to find out yet.”

He immediately looked horrified. “I wasn’t supposed to find out—oh my god—was this a secret? I didn’t mean to—I just—I saw the tea and the crackers and you’re glowing a little and—"

“Bob,” you laughed, “it’s okay.”

He relaxed slightly, cheeks flushed. “Does Bucky know?”

“Not yet.”

Bob pressed his lips together. Then nodded. “I won’t say a word.”

You smiled. “Thanks, Bob.”

He hesitated. Then softly, genuinely, “Congratulations (y/n), you’re gonna be an amazing mum."

And with that, he stood, walked off quietly, and—ten minutes later—came back and wordlessly slid you a chocolate milkshake with a note taped to the cup that read:

“For when the smell finally clears. – Bob”

You stared after him as he walked off, hands in his jacket pockets, head slightly bowed like he hadn’t just completely melted your heart.

Bucky wasn’t supposed to be back yet.

You had counted on at least two more hours, just enough time to hide the half-built, borderline indestructible crib Alexei had wheeled in, distract John before he could bust out his laminated “Uncle Training Schedule,” and maybe, if the stars aligned, finally scrub the yogurt stain off your hoodie.

But the mission ended early. Debrief went faster than expected. And now your husband stood in the doorway of your shared bedroom, still in half his tactical gear, brow furrowed as he took in the scene before him.

There was a crib on the floor, if you could even call it that. John was crouched beside it, cross-legged, a wrench between his knees. Alexei was hammering something loudly and completely unnecessarily.

You were mid-movement, frozen between hiding a pink baby blanket under the bed and whisper-screaming at Alexei to shut up.

Bucky blinked, stepping forward just slightly. “Why is there… furniture in our room?”

“It’s not furniture. It’s a cradle.” Ava replied, almost flatly.

There was a beat. Bucky’s frown deepened. “Why is there a cradle in our room?”

Alexei perked up immediately, beaming, holding up what might’ve once been a baby mobile, now covered in polished throwing stars. “Because you, my friend are going to be papa!”

Silence.

The kind of silence that settled in your bones. Bucky’s eyes scanned the room slowly, the cradle, the weapons-grade mobile, the glittery “CONGRATULATIONS?” banner that Yelena had duct-taped across the headboard. And then, finally, his gaze landed on you.

He looked confused. Careful. Like he couldn’t quite trust what he was seeing.

His voice came soft, hesitant. “You’re… what?”

Your heart was hammering. You took a breath and straightened slowly, hands behind your back, nerves thrumming through your fingertips. “I was going to tell you,” you said gently. “I had a plan. There were cupcakes. A playlist.”

Bucky blinked, still reeling.

John, who had been trying very hard to fade into the wallpaper, raised a hand slightly and said, “Yelena ruined the cupcakes.”

You turned your head slowly. “John.”

“She punched one!” he said quickly.

“It had a baby face on it." Bob quipped.

Yelena’s voice floated in from the hallway. “It was smiling at me wrong!”

Bucky blinked, trying, and failing, to process any of it. His eyes drifted back to you, still full of questions, still locked somewhere between shock and awe.

And then you reached for his hands. Everything softened.

You stepped toward him slowly, reaching for his hands. He let you take them without hesitation, but still stared down at them like they didn’t quite belong to him yet.

“I didn’t want to drop this on you before a mission,” you said softly. “I wanted to wait until it felt like our moment. Something small and quiet. Just us.”

Another beat of silence. And then something shifted.

His shoulders dropped. His hands tightened around yours.

Then he looked up, and everything changed.

You watched it all happen in real time. The realisation, the wonder and the warmth. His features softened, lips parting as his eyes filled with something impossibly tender. Awe bloomed like sunlight breaking through storm clouds.

“You’re really having my baby,” he whispered, like the words alone could undo him.

Your throat tightened. “I’m really having your baby.”

He moved before you could say another word. One hand came up to cradle your cheek, the other curling around the small of your back as he kissed you—softly at first, then deeper, slower. Like he wanted to memorise the moment through touch, like he was anchoring himself in you.

When he pulled back, his eyes were glassy. His forehead pressed against yours, breath trembling.

“I didn’t know I could love you more than I already did,” he murmured. “But you proved me wrong.”

You smiled through the tears. “That’s my job.”

His hands slipped to your waist, pulling you against him fully. One palm eased down to rest over your stomach, warm and steady, and stayed there.

You could feel it in the way his thumb moved—small, gentle strokes over the fabric. Like he was already in love with the tiny life growing there.

A shaky laugh escaped him, part joy, part disbelief. “We’re gonna be parents.”

“Yeah,” you whispered. “We are.”

He kissed your forehead. Then your nose. Then your cheek. He couldn’t stop touching you, holding you, grounding himself in every tiny, real part of this.

You let yourself lean into it, into him, feeling more whole than you ever had in your life.

"God, I love you". Bucky said softly.

“Even after I’ve eaten yogurt-dipped pickles?” you teased gently, chin tilted up.

He pulled back just enough to raise an eyebrow. “That was you?”

“Still recovering from that." John mumbled.

Alexei cleared his throat dramatically. “I play anthem now?”

Yelena appeared in the doorway, cupcake in one hand, "Come on guys, let them have their moment.”

Bucky glanced around the room, eyes still soft but amused. “Wait. You all knew?”

Every head nodded.

He let out a slow, incredulous laugh and looked down at you again, full of something so warm it made your knees wobble.

“Well, damn,” he whispered. “Guess I’m the last to know.”

You smiled, eyes shimmering. “Yeah, but you’re the first to feel our baby kick.”

And right then, perfect, almost surreal, you felt it.

A flutter beneath his hand. A tiny, impossible shift.

His breath caught. His gaze snapped to yours. “Was that—?”

You nodded, tears spilling. “Yeah.”

“Oh my god,” he whispered, dropping to his knees in front of you, hand still over your stomach, lips brushing gently against the space just below your navel. “Hi, sweetheart. It’s me. I’m your dad.”

You laughed through your tears, fingers threading through his hair as your team stood quietly in the background, letting the room finally fall into peace.

And in that moment, with his hand on your belly, your heart in his hands, and the promise of forever in the air, Bucky looked up at you like you were his whole future.

Because you were.

[blueoaknx]

Mitochondrial Dysfunction in Endometriosis

 A Technical Overview of Cellular Mechanisms

Endometriosis, a common gynecological condition affecting approximately 10% of women during their reproductive years, is characterized by the presence of endometrial-like tissue outside the uterine cavity, most frequently in the ovaries, fallopian tubes, and peritoneal cavity. This ectopic tissue leads to a chronic inflammatory environment, pain, and infertility. While the pathophysiology of endometriosis is not fully understood, recent studies have increasingly highlighted mitochondrial dysfunction as a central feature of the disease. This technical article provides a detailed exploration of the role of mitochondria in endometriosis, examining the molecular and cellular mechanisms through which mitochondrial dysfunction contributes to disease progression.

Mitochondrial Function and Metabolism

Mitochondria are dynamic organelles responsible for numerous vital cellular processes, most notably ATP production through oxidative phosphorylation (OXPHOS). ATP is generated within the mitochondrial matrix by the electron transport chain (ETC), which involves the transfer of electrons from NADH and FADH2 to oxygen molecules, ultimately producing ATP. In addition to ATP production, mitochondria are involved in the regulation of calcium signaling, the maintenance of cellular redox balance, apoptosis, and the synthesis of key metabolites, including lipids and steroids. Mitochondria also contain their own genome (mitochondrial DNA or mtDNA), which encodes essential components of the ETC and mitochondrial protein synthesis machinery.

Mitochondria maintain their function through a balance of fusion and fission, processes that help ensure the organelle's shape, distribution, and response to stress. Mitochondrial dysfunction can arise from an imbalance in these processes, as well as from damage to mitochondrial DNA (mtDNA), excessive reactive oxygen species (ROS) production, and impaired bioenergetic functions. In the context of endometriosis, these disruptions have profound implications for cellular homeostasis and tissue function.

Mitochondrial Dysfunction in Endometriosis

In endometriosis, altered mitochondrial function contributes significantly to the disease's pathology. The following mechanisms are central to understanding how mitochondrial dysfunction drives the progression of endometriosis:

1. Altered Metabolic Shifts: The Warburg Effect

A hallmark of cancerous and proliferative cells is a shift in cellular metabolism, often referred to as the Warburg effect, in which cells preferentially utilize glycolysis over oxidative phosphorylation for ATP production, even in the presence of oxygen. This metabolic reprogramming is also observed in endometriotic cells, particularly in ectopic lesions, where cells exhibit increased glycolytic activity. In these lesions, endometrial cells rely less on mitochondrial OXPHOS and instead preferentially use glycolysis for ATP production, generating lactate as a byproduct.

This metabolic shift supports enhanced cell proliferation and survival under suboptimal conditions, characteristic of the hyperplastic nature of endometriosis. Glycolysis is less efficient in terms of ATP production compared to OXPHOS, yet it provides the necessary metabolic intermediates for cell division and biosynthesis. Additionally, the accumulation of lactate in the extracellular space lowers the local pH, which can exacerbate tissue inflammation and create a microenvironment conducive to the growth and persistence of ectopic lesions.

2. Mitochondrial DNA Damage and Instability

Mitochondria are highly susceptible to damage due to their proximity to ROS-producing processes in the electron transport chain. ROS, which are byproducts of cellular respiration, can damage mitochondrial lipids, proteins, and most notably, mitochondrial DNA (mtDNA). Unlike nuclear DNA, mtDNA is not protected by histones, making it particularly vulnerable to oxidative damage. In endometriosis, there is compelling evidence that mtDNA is significantly damaged in ectopic endometrial tissue. Studies have shown mtDNA deletions, mutations, and increased levels of mtDNA fragmentation in these tissues, which suggest a breakdown in the integrity of mitochondrial function.

The damaged mtDNA further exacerbates mitochondrial dysfunction, impairing the ability of mitochondria to generate ATP through OXPHOS. This, in turn, results in an increased reliance on anaerobic glycolysis, fueling the Warburg effect. Furthermore, mtDNA mutations can impair mitochondrial protein synthesis, leading to dysfunctional mitochondrial complexes and altered cellular bioenergetics, perpetuating a cycle of cellular dysfunction in endometriotic lesions.

3. Oxidative Stress and Inflammation

One of the critical roles of mitochondria is the regulation of cellular redox balance. Under normal conditions, mitochondria produce ROS as part of the electron transport chain. However, when mitochondrial function is compromised—whether due to damage, oxidative stress, or metabolic reprogramming—excess ROS are produced, leading to a state of oxidative stress. In endometriosis, ectopic endometrial tissue exhibits elevated levels of ROS, contributing to a persistent inflammatory environment.

Oxidative stress in endometriotic lesions is amplified by mitochondrial dysfunction and is further exacerbated by the Warburg effect, which generates additional ROS during glycolysis. ROS directly activate inflammatory pathways, particularly through the nuclear factor-kappa B (NF-κB) signaling pathway, leading to the production of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α. These cytokines perpetuate the inflammatory response, recruiting immune cells to the site of ectopic lesions, which leads to pain, fibrosis, and the development of adhesions.

Moreover, ROS play a critical role in sensitizing nociceptors, contributing to the chronic pain experienced by women with endometriosis. The interplay between oxidative stress and inflammation forms a vicious cycle that fuels the progression of endometriosis and promotes the growth and persistence of ectopic lesions.

4. Impaired Mitochondrial Dynamics: Fragmentation and Dysfunction

Mitochondria undergo constant fusion and fission, processes that regulate mitochondrial morphology, quality control, and function. Fusion allows for the mixing of mitochondrial contents, which can help dilute damaged components, while fission helps eliminate dysfunctional mitochondria through mitophagy. In endometriosis, there is evidence of disrupted mitochondrial dynamics, particularly an increase in mitochondrial fragmentation. Fragmented mitochondria are less efficient at ATP production and more prone to accumulating damaged proteins and lipids, which further impairs mitochondrial function.

The imbalance between mitochondrial fusion and fission in endometriosis is linked to altered expression of key proteins such as mitofusins (MFN1/2) and dynamin-related protein 1 (DRP1). DRP1-mediated mitochondrial fission is upregulated in endometriotic lesions, contributing to the generation of fragmented mitochondria. These fragmented organelles are associated with increased oxidative stress, apoptosis resistance, and enhanced cell proliferation—features that contribute to the pathogenesis of endometriosis.

5. Apoptosis Resistance and Cell Survival

Mitochondria play a pivotal role in regulating apoptosis through the release of pro-apoptotic factors, such as cytochrome c, from the mitochondrial intermembrane space. These factors initiate the caspase cascade, leading to cell death. However, in endometriosis, ectopic endometrial cells exhibit resistance to apoptosis, allowing them to survive and proliferate abnormally.

Mitochondrial dysfunction in endometriosis leads to alterations in key apoptotic proteins, including Bcl-2 family members, which regulate mitochondrial outer membrane permeabilization (MOMP). The overexpression of anti-apoptotic proteins, such as Bcl-2 and Bcl-xL, and the downregulation of pro-apoptotic proteins, such as Bax and Bak, result in the persistence of damaged cells. This resistance to apoptosis allows for the survival of endometriotic lesions in hostile environments, contributing to the chronic nature of the disease and complicating treatment strategies.

Therapeutic Implications: Targeting Mitochondrial Dysfunction

Given the central role of mitochondrial dysfunction in endometriosis, therapeutic approaches targeting mitochondrial function hold promise for improving disease management. Several potential strategies include:

Antioxidant Therapies: Reducing oxidative stress through antioxidants such as N-acetylcysteine (NAC), Coenzyme Q10 (CoQ10), and vitamin E could help restore mitochondrial function and reduce inflammation in endometriotic tissues.

Modulation of Mitochondrial Dynamics: Targeting proteins involved in mitochondrial fusion and fission, such as DRP1 and MFN2, may help restore mitochondrial morphology and improve bioenergetic function in endometriotic lesions.

Inhibition of Glycolysis: Given the shift toward glycolysis in endometriotic cells, inhibiting key glycolytic enzymes, such as hexokinase or lactate dehydrogenase, may help reduce lesion growth and metabolic reprogramming.

Mitochondrial Biogenesis Stimulation: Activators of PGC-1α, a central regulator of mitochondrial biogenesis, could promote the generation of healthy mitochondria and improve overall cellular metabolism in endometriotic tissue.

Conclusion

Mitochondrial dysfunction is a key contributor to the pathogenesis of endometriosis. Alterations in mitochondrial metabolism, oxidative stress, mitochondrial DNA damage, and impaired apoptotic regulation are central to the disease's progression. Understanding the molecular mechanisms underlying mitochondrial dysfunction in endometriosis provides novel insights into potential therapeutic strategies. Targeting mitochondrial function and bioenergetics could lead to more effective treatments for endometriosis, alleviating its symptoms and improving outcomes for affected women.

[bluepoodle7]

#Target#TargetGoodAndGatherProteinPackTurkeySausageAndColbyJackCheeseQuickBites#TurkeySausageAndCheeseSnack#SnackKitsReview

These Target Good And Gather Protein Pack Turkey Sausage And Colby Jack Cheese Quick Bites were pretty good.

The turkey sausage was firm and soft while lightly chewy in texture.

The turkey sausage had a light turkey poultry flavor that was lightly salty in flavor.

The colby jack cheese was were smooth and creamy in texture while lightly soft in texture.

The colby jack cheese had a light creamy milk taste.

The cheese were little firm and soft in texture with a light salty taste.

This snack kit was lightly salty but not overly salty.

I would eat these again.

Got at Target.