#or abnormal morphology

[fertilitytreatmentpune]

Which is the best IVF center in Pune?

Determining the "best" IVF center in Pune can depend on various factors, including success rates, expertise of the medical team, patient care, facilities, and individual preferences. While I can't definitively label one center as the absolute best, I can suggest a few renowned IVF centers in Pune:

Nova IVI Fertility:

Embrio IVF Centre:

Silverberries IVF Clinic:

Cloudnine Fertility:

Oasis IVF Centre:

Before choosing an IVF center, it's crucial to research each option thoroughly, consider factors such as success rates and patient reviews, and schedule consultations to discuss your specific needs and concerns with the medical team.

[mattbenhews]

What Causes Male Infertility? 10 Common Reasons Explained

 When it comes to infertility, the focus often falls on women, but male infertility is just as significant and affects millions of men worldwide. In fact, about one in every five couples struggling with infertility may have a male factor contributing to the challenge. Let’s dive into the 10 most common causes of male infertility. Whether you’re seeking answers for yourself or someone close to you, understanding these causes is the first step toward finding solutions.

1. Low Sperm Count (Oligospermia)

A low sperm count is one of the most common causes of male infertility. Normal sperm count ranges from 15 million sperm per milliliter to over 200 million. If a man has fewer than 15 million sperm per milliliter, the chances of conception decrease significantly. Low sperm count can be caused by hormonal imbalances, genetic factors, or environmental exposures.

2. Poor Sperm Motility (Asthenozoospermia)

Sperm motility refers to the ability of sperm to swim efficiently toward an egg. Poor sperm motility is another leading cause of male infertility. If the sperm cannot swim effectively, they may struggle to reach and fertilize the egg, reducing the chances of conception. This can result from lifestyle choices, infections, or structural issues in the reproductive organs.

3. Abnormal Sperm Morphology (Teratozoospermia)

Sperm morphology is the study of the size and shape of sperm. Sperm with abnormal morphology (irregular shape or size) can have difficulty reaching and penetrating an egg. This condition may be linked to genetic factors, environmental toxins, or certain health conditions such as diabetes.

4. Varicocele

A varicocele is the enlargement of veins within the scrotum, similar to varicose veins that occur in the legs. It can interfere with the temperature regulation of the testicles, causing sperm production to decrease. Varicoceles are found in about 15% of the general male population but can be responsible for up to 40% of cases of male infertility.

5. Erectile Dysfunction (ED)

Erectile dysfunction, the inability to achieve or maintain an erection sufficient for sexual intercourse, can significantly impact fertility. While ED does not directly affect sperm quality, it hinders the physical ability to ejaculate during intercourse. Causes of ED include psychological factors, health conditions (e.g., diabetes), or side effects from medications.

6. Testicular Ailments (Infections or Injury)

Infections such as epididymitis, orchitis, and sexually transmitted infections (STIs) can impact sperm production and function. Testicular injuries or surgeries can also damage sperm-producing cells, leading to infertility. Conditions like mumps, if contracted after puberty, can also affect the testicles and lead to permanent infertility.

7. Hormonal Imbalances

Hormones play a crucial role in sperm production. An imbalance in hormones like testosterone, thyroid hormone, or prolactin can disrupt the production of sperm. Conditions such as hypogonadism (low testosterone levels), obesity, or pituitary gland problems can lead to hormonal imbalances that affect male fertility.

8. Genetic Factors

Genetics can significantly influence male fertility. Conditions such as Klinefelter syndrome (an extra X chromosome), Y-chromosome microdeletions, or cystic fibrosis can lead to infertility. In some cases, genetic abnormalities affect the production or function of sperm, while in others, they affect the structure of the reproductive organs.

9. Lifestyle Factors

Smoking, excessive alcohol consumption, recreational drug use, and poor diet can all decrease sperm quality. Regular physical activity is essential for maintaining overall health, but excessive exercise or heat exposure (such as frequent use of saunas or hot tubs) may negatively impact sperm production.

10. Environmental and Occupational Factors

Exposure to environmental toxins and chemicals, such as pesticides, heavy metals, or industrial chemicals, can impair sperm production. Men working in occupations involving exposure to toxic substances, such as welding or chemical manufacturing, may have a higher risk of infertility. Similarly, radiation and prolonged exposure to high temperatures can also decrease sperm count and quality.

Early intervention, lifestyle changes, and medical treatments are often effective in overcoming male infertility. For those looking for expert care, Prashanth IVF offers the best treatment options for male fertility, with a team of specialists dedicated to providing personalized, cutting-edge solutions.

[cardiacreports2]

Autopsy Report

Case Number: 2024-1125-01 Decedent Name: Chad Evanston Age: 19 Sex: Male Height: 5’11” Weight: 154 lbs (estimated lean build) Race/Ethnicity: Caucasian Date of Death: November 24, 2024 Time of Autopsy: November 25, 2024, 9:00 AM Pathologist: Dr. Robert Linfield

I. External Examination

General Appearance: The decedent is a well-developed, lean, and athletic-appearing 19-year-old male, weighing approximately 154 pounds. He has brown hair, approximately 3 inches in length, and brown eyes. Skin is pale but otherwise unremarkable, with no evidence of external trauma or defensive injuries. Fingernails are clean and well-trimmed.

Clothing: The decedent was found dressed in athletic attire, including a blue baseball cap, black athletic shorts, a running watch on the left wrist, and well-worn running shoes. The clothing was damp due to environmental exposure but showed no tears or stains of significance beyond expected post-mortem findings.

Identifying Marks: A faint scar measuring 2 cm is present on the left knee, consistent with prior minor trauma or surgery. No tattoos or other distinguishing marks.

II. Internal Examination

Cardiovascular System: The heart is notably abnormal upon inspection. Weighing 390 grams (upper end of normal for the decedent's size and build), the heart exhibits significant thickening of the left ventricle (left ventricular hypertrophy). The mitral valve shows marked structural abnormalities, including:

Fibrotic thickening of the leaflets.

Mild calcification at the annulus.

Evidence of prolapse of the posterior leaflet, causing incomplete coaptation during closure. This structural defect resulted in significant mitral regurgitation, which would have led to reduced cardiac efficiency during exertion.

Examination of the coronary arteries reveals no signs of atherosclerosis or narrowing. However, microscopic examination identifies mild interstitial fibrosis in the ventricular myocardium, particularly in the left ventricle. These findings are consistent with chronic strain and early-stage cardiomyopathy, likely exacerbated by prolonged high-intensity physical activity.The conduction system shows mild scarring near the sinoatrial node, likely the origin of the arrhythmias detected on the decedent's running watch.

Lungs: The lungs weigh 520 grams (right) and 480 grams (left), with mild congestion. Examination shows no emboli or aspirated material.

Abdominal Organs: All abdominal organs, including the liver, spleen, kidneys, and gastrointestinal tract, appear normal in size and morphology.

Brain: Examination of the brain reveals no hemorrhages, infarcts, or structural abnormalities.

III. Microscopic Findings

Heart Tissue: Histological examination of the heart confirms chronic myocardial fibrosis and focal areas of myocyte disarray. These findings are indicative of longstanding structural abnormalities and stress-induced cardiac remodeling.

Lung Tissue: Pulmonary alveoli appear congested but otherwise unremarkable.

Valvular Tissue: Fibrosis and calcification of the mitral valve tissue are evident, along with cellular degeneration, consistent with a congenital or acquired valvular defect exacerbated over time.

IV. Toxicology Report

Testing for substances, including recreational drugs, alcohol, and common stimulants, returned negative results.

V. Cause of Death

Sudden cardiac arrest secondary to severe mitral valve dysfunction and associated arrhythmia.

Detailed Analysis of Cardiac Findings

The decedent's heart exhibited chronic and progressive mitral valve disease. The fibrotic and calcified changes in the mitral valve likely originated from an undiagnosed congenital defect, aggravated over time by physical exertion. The incomplete closure of the mitral valve resulted in backflow of blood (regurgitation) during systole, progressively overloading the left atrium and left ventricle. Over time, this stress led to the observed hypertrophy and scarring of the myocardium.

The combination of myocardial fibrosis and conduction system scarring predisposed the decedent to severe arrhythmias. The running watch data corroborates this, showing prolonged arrhythmic episodes throughout the decedent's final run.

The sustained stress of a nine-mile run caused the decedent’s heart to become electrically unstable, leading to ventricular fibrillation—a fatal arrhythmia resulting in sudden cardiac arrest. The autopsy findings, supported by wearable device data, confirm that this event was precipitated by his preexisting cardiac abnormalities.

Despite being otherwise healthy and athletic, the decedent’s heart was structurally compromised, making high-intensity exercise particularly dangerous. The mitral valve's dysfunction was significant enough that even mild to moderate exertion may have posed a risk over time.

Conclusion: Chad Evanston’s death was due to undiagnosed and progressive cardiac pathology exacerbated by prolonged physical exertion. This case highlights the critical need for screening individuals engaging in high-intensity activities for underlying heart conditions.

Final Manner of Death: Natural

[spoonbendersanonymous]

I am extremely picky about anime because my patience for anime bullshit is incredibly low, so I've only ever watched a handful of them and I've only ever watched one all the way through (Soul Eater) but I have zoology degree and work at a zoo so I obviously have watched the Furry Anime(tm) (Beastars).

I love the animation style and music, but I definitely have some issues with the writing. But I'm not here to talk about that. I'm here to complain about exactly one big nitpick I have because I'm a nerd about animal morphology.

So throughout the anime I feel like some of the herbivore species are portrayed as inherently really weak compared to carnivorous species, which is kind of bs if you think about it. Like I get it, a sheep and a bunny aren't going to stand up to something like a lion or a grizzly bear, and there are also examples of herbivores being able to stand up to predators (herbivores in the police force, the crime fighting horse that kills lions, etc.). My point is that a lot of herbivorous species could absolutely kick a carnivore's ass, no guns required.

My biggest issue, however, is with Louis, canonically a red deer, being portrayed as a skinny little twink compared to a grey wolf. I get it, it's part of the conflict he's dealing with, but also red deer are fucking HUGE.

Look at this fucking thing. It's a deer the size of an elk. Males can weigh up to 530 pounds while male grey wolves are around 180 at the absolute largest. A single grey wolf isn't gonna take one of these guys down without getting seriously hurt by those antlers and hooves. Wolves can take down adult moose, but only in a relatively large pack. They're also close to twice the height of an adult male grey wolf (around 51 in at the shoulder). Louis should be towering over Legosi, even with him being abnormally tall for a wolf. If they wanted a smaller, weaker deer I'd say make Louis a whitetail deer or fallow deer, not one of the largest deer species in the world.

Anyway yeah Louis should not be portrayed as a twink imo and he could kick the gay wolf's ass like 9 times out of ten. The guy should look like a gym bro or something.

[valkyries-things]

DR. MARTHE GAUTIER // RESEARCHER

“She was a French medical doctor and researcher, best known for her role in discovering the link of diseases to chromosome abnormalities. She worked at Trousseau Hospital in Raymond Turpin’s team. Turpin's research was focused on polymalformative syndromes, of which the most common is trisomy, characterized by intellectual disability and morphological abnormalities. At the time, Turpin favored the hypothesis of a chromosomal origin of trisomy but there was no laboratory for cell culture in France and the number of human chromosomes was estimated at 48, but without any certainty. She entrusted her research to Jérôme Lejeune, who offered to take pictures in another laboratory better equipt, however he did not return the slides of research, but instead reported the discovery as his own.”

[way2manyusernamez]

i feel like lately i've taken a small step back from this account and focused on other things in my life. here's my thoughts on this "radqueer-adjacent / paraphilia / transID / shipcourse" stuff:

i like the anti-contact paraphilia acceptance/education movement. i feel thankful for it; it helped me understand myself better and changed how i view abnormal attractions.

i’m still pro morphological freedom. i guess i'm still pro-transID because i don't have an issue with the term. (i don't like any of the alternatives more.) i feel like this has also helped me understand myself better

i’m still pro fiction (expressing philias through fiction, exploring dark topics through fiction; properly tagging). i like criticizing media and its effect on the world though

i’m anti contact: don’t try to have sex with kids, or (non-human biological) animals, try to be respectful of peoples corpses even if nobody is living in them any more, don’t rape people... (i think it's unfortunate that this needs to be said, but if you don't try to push pro-contact ideology away, it'll take over a community. this is what i think might have happened with the radqueer community to some degree, becoming more pro c / apathetic over time. or maybe it was always kinda bad and i just don't remember lol)

i’m tired of contact neutrality and i don’t like how contact-neutral the radqueer community is. my hot take: "making a safe space for everyone" is bad when "everyone" includes rapists (a safe space for abusers to be abusive = not a safe space for (possible) victims). it really gives me bad vibes when someone posts about paraphilias a lot, but doesn’t say anything about their opinions on if it’s bad to abuse animals/children. being against harmful contact is crucial to me.

i don’t really consider myself radqueer any more. but i’m still pro paraphilia and pro transID, so i don’t really feel like calling myself “anti radqueer” either, since that usually means ‘against transIDs or paraphilias in some way’. i'm not really "for" or "against" radqueer as a concept - i just don't like the community much any more. it's probably partly because i have grown more skeptical/critical of "contact neutrals", and also partly because it's just gotten worse in general from what i can remember.

i would really like to have more people in the world that are pro morphological freedom and pro para (skeptical of repression and "recovery" that's just trying to change the attraction, but anti contact). maybe that's an overly specific dream, lol.

[ask-a-vetblr]

Well, my cat passed away a month ago and I would like to understand what happened to her (or at least just understand what a gastrointestinal lymphoma could've done to make her have a systematic inflammation issue in her endocrine system.) I couldn't get a straight answer from any of the vets I asked. They only said it was the cancer. I just want to understand. I've been researching and I didn't find anything like that. She was on antibiotics.

Hi, Sueanoi here.

Condolences to your loss. It is incredibly difficult to give a straight answer on a specific cause of death without necropsy (veterinary's word for animal autopsy). However, I could attempt to guess.

Lymphoma, or any cancer at all really, is an uncontrolled growth of abnormal cells. Anywhere that it grows, it disrupt the normal function of that organ. Many cancers are notorious for being able to spread to other organs than its origin. Thus, if it jumps from GI tract to ... let's say pancreas, (which is one nearby endocrine organ), it can cause a catastrophic failure of everything that the pancreas is supposed to do.

Lymphoma is already a cancer of immune cells. It is tightly linked to inflammation. Blood result can look indistinguishable from a sepsis, unless a manual blood smear is performed so the morphology of the white blood cells are checked.

I'm so sorry, but there are so many ways a body can fail in a case like this. This is the closest guess I could provide, I hope this will help you find some closure.

[tribbetherium]

'The dawn rays of the rising suns highlight the imperfections of nature's workings as a pair of female pterowrists, emerging at first light, prowl among the burrows of a colony of marmoths in the hope of picking off a straggler when they surface to forage. Yet something peculiar is immediately noticeable with one of them, her stunted size compared to her partner and her asymmetrical, elongated left wing marking her as something incredibly rare: she is a gynandromorph, a rare aberration produced by a chromosomal anomaly that results in an organism with a chimeric patchwork of male and female traits. This trait is also found in other species, but nowhere is it as visually dramatic as in a species with such an extreme sexual dimorphism as the pterowrist: producing such bizarre morphologies that greatly affect the ontogeny of the creature with its abnormal hormonal signals. This individual, however, seems quite prosperous in spite of it all: managing to survive to adulthood and adjust to her lopsided anatomy. Even so, she will never reproduce, or pass on her unusual trait: her hormonal signals have made her behavior in that she is attracted instead to the scent of another female, and even otherwise cannot produce viable egg cells with her impaired chromosomes that interfere with meiosis. Though an individual success, managing to reach such an age despite a physical anomaly, she ultimately is but a rare sporadic fluke-- produced mistakenly with extreme rarity and a dead end for the genes that made her so.'

--------

[deeplorewhore]

So you heard how countryhumans were made… mythologically

Now to hear what science has to say.

Countryhumans' scientific name is Homo terra, under the genus Homo. All Homo terra have a form of defensive form, used to protect themselves and their people and triggered by danger. Mythologically, their primary diety Pangaea had the foresight to know that Her children would need such a thing, so She granted them such power. Science, however, begs to differ. Defensive forms, in fact, are what was used to trace the origins of Homo terra.

—

Once they were manifestations of the raw cooperative energy created by humans working together in large, meta-familial groups. They were nebulous in morphology, taking on whatever form was most appealing to the group they represented. They co-existed, and eventually co-evolved with Homosapiens, growing to depend on them more for continued survival. How human social energy became sentient and sapient is still unexplained.

—

Eventually, these manifestations began to take on Homosapien forms, but not because they decided to willingly take on a permanent, anthropomorphic embodiment. Their ancestors began to intermingle more with humans, including reproductively. Once again, it remains unknown how Homo terra ancestors reproduced successfully with Homo sapien. They eventually fell under the genus Homo, with their original energy form being unknown. Now, Homo terra are visually nearly indistinguishable from other humans, with the exception of features like wings, horns, or tails, as well as abnormal sizes and adaptive internal organs.

—

Each Homo terra is equipped with a defensive form that is mostly controlled by fear and danger responses. This was an evolutionary advantage from their ancestors that remained after their merge with homosapien. Another evolutionary advantage from their ancestors is their extreme durability, regenerative ability, and incredibly long lifespans. Homo terra genes are being used to regenerate limbs and organs of humans, with mixed results.

--

This theory is also proposed to explain why some Homo terra are “born” from social necessity or by chance, but evolutionary biologists still have yet to explain why they would not be more alike their ancestors in morphology. While it has not been discovered how the infamous "blood and earth" method works to reproduce, biologists suspect it has something to do with special properties of their blood, linked to Homo terra's regenerative abilities.

--

Belief in Pangaea remains prolific as an explanation to the scientifically unexplained, a God-of-the-Gaps.

[glamnotes]

Abnormalities in RBC Morphology

[mcatmemoranda]

Going through the ACLS online training:

The P wave represents depolarization of the atrial myocardial cells.

The PR interval represents the time from the beginning of atrial depolarization to the beginning of ventricular depolarization. It is measured from the beginning of the P wave to the beginning of the QRS complex. The normal duration of the PR interval is 120 to 200 milliseconds.

The QRS complex represents depolarization of the ventricular myocardial cells. The normal duration of the QRS complex is less than 120 milliseconds.

The J point is the point where the QRS complex ends and the ST segment begins.

The T wave represents repolarization of the ventricular myocardial cells. (Atrial repolarization occurs during ventricular depolarization and is not seen on the ECG; it is overshadowed by the depolarization of the larger ventricles).

The QT interval is measured from the beginning of the QRS complex to the end of the T wave. This encompasses the time from ventricular depolarization to the end of repolarization.

The ST segment represents the time between the end of ventricular depolarization and the beginning of ventricular repolarization. It is measured from the end of the QRS complex to the beginning of the T wave.

Is the amount of time between each P wave the same? What about the amount of time between each QRS complex (i.e., the RR interval)?

To estimate the atrial rate, count the number of P waves over a 6-second period and multiply by 10. To estimate the ventricular rate, do the same with the QRS complexes. Alternatively, if the rhythm is regular, divide 300 by the number of large squares between two P waves (to get the atrial rate) and between two R waves (to get the ventricular rate). If the heart rate is very fast, divide 1500 by the number of small squares between two P waves (to get the atrial rate) and between two R waves (to get the ventricular rate). Are the atrial and ventricular rates the same or different? Are they within normal limits?

Look for the P waves. Are they there? Do all the P waves have the same morphology? Is there one––and only one––P wave associated with each QRS complex? Note that in lead II, the P waves are usually upright but in lead V1, the P waves may be inverted or biphasic.

Measure the QRS complex. Is it within the normal range? (QRS complexes that exceed 120 milliseconds in duration are abnormal.) Do all the QRS complexes have the same morphology?

Look for the T waves. Are they there? If so, do all the T waves have the same morphology? The direction of the T wave should be the same as that of the main vector of the QRS. The T waves should be less than 5 millimeters in amplitude in the limb leads and less than 15 millimeters in amplitude in the precordial leads.

Measure the PR interval. Is it within the normal range? Is it consistent throughout the tracing? If it varies, is the variation predictable?

Measure the QT interval and calculate the corrected QT interval. Because the QT interval varies normally with the heart rate, the corrected QT interval (QTc) is used to give a value that is theoretically independent of rate. The QTc adjusts for heart rate differences by dividing the QT interval by the square root of the RR interval (i.e., one cardiac cycle). In general, a QTc greater than 460 milliseconds is considered to be prolonged. If the heart rate is faster than 120 bpm or slower than 50 bpm, the formula for calculating the QTc is not considered valid and should not be used.

Look at the ST segment. Is it elevated or depressed from the baseline?

Determine the rhythm and its clinical significance. Is the patient showing signs or symptoms? Is the rhythm potentially life-threatening?

In normal sinus rhythm:

Each P wave is linked in a 1:1 fashion to each QRS complex (i.e., atrial depolarization is always linked to ventricular depolarization).

The P waves are uniform in shape, indicating that the SA node is the only pacemaker driving atrial depolarization.

P waves in lead II are normally upright and all the same shape. P waves in lead V1 are normally inverted (or on occasion biphasic) and all the same shape.

The rhythm is regular (but may vary slightly during respirations).

The rate ranges between 60 and 100 bpm.

Causes of sinus bradycardia include:

Vagal stimulation.

Myocardial infarction.

Hypoxia.

Medications (e.g., β-blockers, calcium channel blockers, digoxin).

Coronary artery disease.

Hypothyroidism.

Iatrogenic illness.

Inflammatory conditions.

First-degree AV block is characterized by a prolonged delay in conduction at the AV node or bundle of His. The impulse is conducted normally from the sinus node through the atria, but upon reaching the AV node, it is delayed for longer than the usual 0.2 second. In first-degree AV block, although the impulses are delayed, each atrial impulse is eventually conducted through the AV node to cause ventricular depolarization.

First-degree AV block may be a normal finding in athletes and young patients with high vagal tone. It can also be an early sign of degenerative disease of the conduction system or a transient manifestation of myocarditis or drug toxicity.

In second-degree AV block type I (also called Mobitz type I or Wenckebach block), impulses are delayed and some are not conducted through to the ventricles. After three or four successive impulse delays, the next impulse is blocked. After the blocked impulse, the AV node resets, and the pattern repeats. Second-degree AV block type I usually occurs at the AV node but may be infranodal.

Because the block usually occurs above the bundle of His, conditions or medications that affect the AV node (such as myocarditis, electrolyte abnormalities, inferior wall myocardial infarction or digoxin) can cause second-degree AV block type I. This type of arrhythmia can also be physiologic.

Second-degree AV block type I rarely produces symptoms. Some patients may have signs and symptoms similar to sinus bradycardia.

In second-degree AV block type II (Mobitz type II), the block occurs below the AV node, in the bundle of His. As with second-degree AV block type I, some atrial impulses are conducted through to the ventricles, and others are not. However, there are no progressive delays. The blocked impulses may be chaotic or occur in a pattern (e.g., 2:1, 3:1 or 4:1). In high-grade second-degree AV block type II, the ratio is greater than 2:1 (i.e., 3:1, 4:1, or variable).

Second-degree AV block type II is always pathologic. It is usually caused by fibrotic disease of the conduction system or anterior myocardial infarction.

Patients may present with light-headedness or syncope, or they may be asymptomatic. The clinical presentation varies, depending on the ratio of conducted to blocked impulses.

In third-degree (complete) AV block, no impulses are conducted through to the ventricles. The block can occur at the level of the AV node but is usually infranodal. Pacemaker cells in the AV junction, bundle of His or the ventricles stimulate the ventricles to contract, usually at a rate of 30 to 45 bpm. This means that the atria and ventricles are being driven by independent pacemakers and are contracting at their own intrinsic rates (i.e., 60 to 100 bpm for the atria and 30 to 45 bpm for the ventricles), a situation known as AV dissociation.

Degenerative disease of the conduction system is the leading cause of third-degree AV block. This arrhythmia may also result from damage caused by myocardial infarction, Lyme disease or antiarrhythmic drugs.

If ventricular contraction is stimulated by pacemaker cells above the bifurcation of the bundle of His, the ventricular rate is relatively fast (40 to 60 bpm) and reliable, and symptoms may be mild (such as fatigue, orthostatic hypotension and effort intolerance). However, if ventricular contraction is stimulated by pacemaker cells in the ventricles, the ventricular rate will be slower (20 to 40 bpm) and less reliable, and symptoms of decreased cardiac output may be more severe.

First-Degree AV Block

In first-degree AV block, normal P waves are followed by QRS complexes, but because the impulse is delayed at the AV node or bundle of His, the PR interval is longer than normal (i.e., it exceeds 200 milliseconds). Each P wave is linked in a 1:1 fashion to each QRS complex. QRS complexes of normal duration suggest that the delay is occurring at the level of the AV node, whereas wide QRS complexes suggest that the delay is infranodal.

Regularity: regular Rate: variable, can occur with normal rate, bradycardia or tachycardia P wave: upright and uniform, one for every QRS complex QRS complex: < 0.12 second PR interval: > 0.20 second

Second-Degree AV Block Type I

Because some impulses are not conducted through to the ventricles, the ratio of P waves to QRS complexes is greater than 1:1. Because each impulse is delayed a little more than the last until eventually one impulse is completely blocked, the ECG shows progressive lengthening of the PR interval with each beat, then a P wave that is not followed by a QRS complex (a “dropped beat”). In most cases, the RR interval decreases before each dropped beat. After the dropped beat, impulse conduction through the AV node resumes and the sequence repeats.

Regularity: irregular in a pattern Rate: variable, usually < 100 bpm P wave: upright and uniform; more P waves than QRS complexes QRS complex: < 0.12 second PR interval: becomes progressively longer until a P wave is not conducted, then cycle repeats.

Second-Degree AV Block Type II

Second-degree AV block type II is characterized by a constant PR interval. Because impulses are intermittently blocked, there are more P waves than QRS complexes.

Regularity: regular (2:1), unless conduction ratio varies Rate: usually < 100 bpm (atrial and ventricular), tendency for bradycardia P wave: upright and uniform; more P waves than QRS complexes (2:1, 3:1, 4:1 or variable) QRS complex: < 0.12 second PR interval: < 0.20 second or prolonged; constant for every QRS complex.

Third-Degree AV Block

In third-degree AV block, there is no electrical communication between the atria and ventricles, so there is no relationship between P waves and QRS complexes. The RR interval is constant. The PP interval is constant or slightly irregular. If pacemaker cells in the AV junction stimulate ventricular contraction, the QRS complexes will be narrow (less than 120 milliseconds in duration). Impulses that originate in the ventricles produce wide, bizarre QRS complexes.

Regularity: usually regular RR interval, regular PP interval Rate: varies depending on escape focus; junctional (40–60 bpm) and ventricular (< 40 bpm) P wave: upright and uniform, more P waves than QRS complexes QRS complex: < 0.12 second if junctional escape, ≥ 0.12 second if ventricular escape PR interval: total dissociation from QRS complexes

Tachyarrhythmias can be categorized as narrow complex or wide complex.

Narrow-complex tachyarrhythmias include sinus tachycardia, atrial flutter, atrial fibrillation and supraventricular tachycardia. These tachyarrhythmias usually originate in the atria or AV node and run normally through the bundle branches, producing a normal QRS complex.

Wide-complex tachyarrhythmias originate in the ventricles and include ventricular tachycardia (monomorphic and polymorphic) and ventricular fibrillation. Supraventricular tachycardia with aberrant conduction can also produce a wide-complex tachyarrhythmia.

Sinus tachycardia is the most common tachyarrhythmia. It is identical to normal sinus rhythm, except the rate is between 100 and 150 bpm.

Atrial flutter is caused by an ectopic focus in the atria that causes the atria to contract at a rate of 250 to 350 bpm. The underlying mechanism of atrial flutter is most often a re-entrant circuit that encircles the tricuspid valve annulus.

Supraventricular tachycardia (SVT) is an arrhythmia originating above the ventricles. In general, the rate is greater than 150 bpm, which helps to differentiate SVT from sinus tachycardia. SVT can be classified as AV nodal re-entrant tachycardia (AVNRT), AV-reciprocating tachycardia (AVRT) and atrial tachycardia.

This rhythm is seen in patients with:

Low potassium and magnesium levels.

Family history of tachycardia.

Structural abnormalities of the heart.

Adverse reactions from certain pharmacologic agents (e.g., antihistamines, theophylline, cough and cold preparations, appetite suppressants).

Certain medical conditions (e.g., cardiovascular disease, long-term respiratory disease, diabetes, anemia, cancer).

Illicit drug use.

Atrial fibrillation is caused by multiple ectopic foci in the atria that cause the atria to contract at a rate of 350 to 600 bpm. Rarely, the atrial rate may be as high as 700 bpm. The AV node only allows some of the impulses to pass through to the ventricles, generating an irregularly irregular rhythm that is completely chaotic and unpredictable.

Atrial fibrillation can occur in young patients with no history of cardiac disease. Acute alcohol toxicity can precipitate an episode of atrial fibrillation in otherwise healthy patients. However, atrial fibrillation commonly occurs in the presence of underlying heart disease, lung disease, hyperthyroidism or myocardial infarction.

Ventricular tachycardia occurs when a ventricular focus below the bundle of His becomes the new pacemaker. The ventricles contract rapidly (usually at a rate faster than 100 bpm) and usually with a regular rhythm. The rapid ventricular rate significantly diminishes cardiac output and can only be sustained for a short period before the patient becomes hemodynamically compromised. Ventricular tachycardia can quickly turn into ventricular fibrillation, leading to cardiac arrest.

In atrial flutter, atrial contraction occurs at such a rapid rate that discrete P waves separated by a flat baseline cannot be seen. Instead, the baseline continually rises and falls, producing the “flutter” waves. In leads II and III, the flutter waves may be quite prominent, creating a “sawtooth” pattern. Because of the volume of atrial impulses, the AV node allows only some of the impulses to pass through to the ventricles. In atrial flutter, a 2:1 ratio is the most common (i.e., for every two flutter waves, only one impulse passes through the AV node to generate a QRS complex). Ratios of 3:1 and 4:1 are also frequently seen.

Regularity: usually regular (could be irregular with variable conduction) Rate: varies with conduction; < 100 bpm is controlled; > 100 bpm is uncontrolled (rapid ventricular response); usually has ventricular rates of 75 bpm (4:1), 100 bpm (3:1) or 150 bpm (2:1), depending on conduction ratio P wave: none; flutter (F) waves; characteristic “sawtooth” baseline QRS complex: < 0.12 second PR interval: not discernible

Supraventricular Tachycardia

In supraventricular tachycardia (SVT), the P waves may be absent or abnormal. There is minimal to no beat-to-beat variability and the heart rate is usually greater than or equal to 150 bpm.

Regularity: regular; minimal beat-to-beat variability Rate: > 150 bpm P wave: absent or not clearly identifiable QRS complex: < 0.12 second PR interval: if P waves are visible, PR interval may be shortened or lengthened depending on mechanism

Atrial Fibrillation

The two key features of atrial fibrillation on ECG are the absence of discrete P waves and the presence of irregularly irregular QRS complexes. The baseline appears flat or undulates slightly, producing fibrillatory waves.

Regularity: irregularly irregular Rate: varies with conduction; < 100 bpm is controlled; > 100 bpm is uncontrolled (rapid ventricular response) P wave: none; fibrillation (f) waves; chaotic baseline QRS complex: < 0.12 second PR interval: not discernible

Monomorphic Ventricular Tachycardia

In ventricular tachycardia, the QRS complexes are wide (lasting longer than 120 milliseconds) and bizarre in shape. When there is only one ectopic focus in the ventricles, monomorphic ventricular tachycardia is seen on the ECG (i.e., the QRS complexes are generally the same bizarre shape). Monomorphic ventricular tachycardia may also be seen with reentrant rhythms.

Regularity: regular Rate: > 100 bpm P wave: not discernible QRS complex: ≥ 0.12 second, uniform in shape PR interval: not discernible

Polymorphic Ventricular Tachycardia

In polymorphic ventricular tachycardia, which occurs when there are two or more ectopic foci, the QRS complexes vary in shape and rate.

Regularity: irregular (can appear regular due to fast rate) Rate: > 100 bpm P wave: not discernible QRS complex: ≥ 0.12 second, variable in shape PR interval: not discernible

[drguptasclinic1]

Unraveling the Enigma: Exploring the Causes of Infertility in Men and Women

Infertility, a condition that affects millions of couples worldwide, can be a source of immense emotional distress and frustration. While there are numerous factors that can contribute to infertility, understanding its underlying causes is essential for effective diagnosis and treatment. In this article, we delve into the multifaceted causes of infertility in both men and women, shedding light on the complex interplay of biological, environmental, and lifestyle factors.

Causes of Infertility in Women

Ovulation Disorders: Irregular or absent ovulation can hinder conception. Conditions such as polycystic ovary syndrome (PCOS), thyroid disorders, and premature ovarian insufficiency (POI) can disrupt the ovulation process.

Fallopian Tube Damage: Blockages or damage to the fallopian tubes can prevent the egg from reaching the uterus for fertilization. Previous pelvic infections, endometriosis, or surgery may contribute to fallopian tube issues.

Uterine Abnormalities: Structural abnormalities in the uterus, such as fibroids or polyps, can interfere with embryo implantation and development, leading to infertility.

Age-related Factors: As women age, the quantity and quality of their eggs decline, making conception more challenging. Advanced maternal age is a significant risk factor for infertility.

Causes of Infertility in Men

Low Sperm Count or Quality: Issues with sperm production, motility, or morphology can impair fertility. Factors such as hormonal imbalances, genetic conditions, and lifestyle choices (e.g., smoking, excessive alcohol consumption) can affect sperm health.

Varicocele: A varicocele, an enlargement of the veins within the scrotum, can lead to decreased sperm production and quality. It is a common reversible cause of male infertility.

Testicular Factors: Conditions such as undescended testicles, testicular trauma, or infections can impact sperm production and function, contributing to infertility.

Ejaculatory Disorders: Disorders affecting the ejaculation process, such as retrograde ejaculation or erectile dysfunction, can hinder the delivery of sperm during intercourse.

Seeking Help from a Male Fertility Doctor

For couples struggling with infertility, consulting a male fertility doctor, also known as a reproductive urologist or andrologist, can provide valuable insights and guidance. These specialists are trained to evaluate and treat male infertility issues, offering diagnostic tests, fertility evaluations, and personalized treatment plans to address underlying causes and improve reproductive outcomes.

Conclusion

Infertility can stem from a myriad of factors affecting both men and women. By understanding the potential causes of infertility and seeking specialized care from a male fertility doctor specialist, couples can embark on a journey towards achieving their dream of parenthood. With advancements in reproductive medicine and personalized treatment approaches, there is hope for overcoming infertility challenges and building a family.

[anomaly-beans]

WAUGHHH

Anyway I used the morphology tool to make a fandragon I would love to get. If I can find colors close enough to it.

I want to make another abnormality based one for porccubus

[calowlmitygoddess]

Tanza Mortal Races

Draki

Here

Humans

Humans are the defacto dominant species of Tanza, morphologically speakin they are exactly the same as real life humans, except they have long, mobile ears. Humans dont have natural bright colours (purple/blue stuff like that) unless they have Drakin ancestry, but human mages who spend a lot of time handling Neautra may come to experience abnormal coloration, usually the eyes, tip of the finguers and hair.

Speaking of Neautra, unlike Drakin that have a natural gift for it, pure blood humans are not able to naturally wield Neautra and must use conduits to cast magic, such as spellbooks (books with ready to use spells written out that simply need to be activated), Jewels made of Crystalized Neautra, or in some more radical cases tatooing spells on the body that allow for instant cast.

Humans form the Izeriath Empire, a very technologically advanced nation, (they have stuff like fantasy internet, magic phones, magic cars etc) as well culturally diverse given its immense size. It spend much of its history struggling to keep itself togheter, tought it has been pretty stable for the past century.

One of the most dark periods in Izerianthi history has been 500 years ago, when a Demon Lord managed to breach into the mortal realm right into the empire's capital, that demon lord started a 20 year reign of terror, mortals had never faced a demon this powerful before, and only thanks to an Izerianthi and Drakin alliance managed to finally slay him.

The Empire had a very closed relationship with the spirits, their archmages were able to communicate and learn their language to master powerful magics, The Imperial Family had a deal with a spirit and blessed by it, and the Gods had a honorary seat at the State Council. It was enjoying a very nice period of stability, until the god Shadlan was killed by a mortal, the spirits turned on them and demon attacks have become more and more common.

[agnol117]

Series I, Part II

SCP-007 - Abdominal Planet

This one kinda scares the hell out of me, to be honest. Not the skip itself (dude with a planet where his abdomen should be, kinda weird, but otherwise fairly tame for an SCP entry). No, what scares me about this one is (and this will be a recurring theme) the way they’re just holding a dude hostage with no real oversight or recourse. Sure, the guy’s SSN comes up as invalid, but still. They’ve got this guy, they’re denying him access to the outside world, and…they’re just gonna get away with it.

As I said, this will be a recurring theme. In a lot of cases, I think the actual containment of things (usually people) is worse than the thing itself.

7/10

SCP-008 - Zombie Plague

This one does nothing for me. It’s exactly what it says on the tin, and while that’s fine, it just doesn’t appeal to me. All the same, I feel hesitant to give it a low rating because it is well written, it just isn’t my thing.

6/10

SCP-009 - Red Ice

This one’s kinda neat. It’s evil water (you can tell it’s evil because it’s red). It can contaminate normal water (including the water in people) and will kill them. It’s probably from another dimension. I don’t have much to say about this one. It’s just a fun concept.

7/10

SCP-010 - Collars of Control

I don’t like this one.

Not conceptually. Conceptually it’s great. Collars that allow whoever has the remote complete control over the wearer as long as they understand how to use the remote is a great concept. I love it. I also hate it, because one of the lines is “The most abnormal feature of the collars is the effect they have on the body morphology. They allow the user of the remote to reconfigure the shape of the victim to an extent that is apparently only limited by the knowledge of the programming language of the remote.” Nope. Hate it. I can take a lot of body horror, but like…something about that sets off all my Nope! Alarms.

9/10

SCP-011 - Sentient Civil War Memorial Statue

This one’s just kinda sweet? Again, it’s exactly what it says on the tin: A Civil War Memorial Statue in Vermont that just happens to be alive and sentient. It’s nice. I liked reading this one.

10/10

[drbendale]

How Does the Quality of Embryos Affect the Success Rates of IVF Procedures?

In Vitro Fertilization (IVF) has emerged as a transformative solution for couples facing infertility. As a complex procedure, IVF involves multiple steps, each critical to achieving a successful pregnancy. Among these steps, the quality of embryos stands out as a significant factor influencing the success rates of IVF procedures. Dr. Pavan Devendra Bendale, a Senior IVF Specialist at Crysta IVF Fertility Center in Pune, has over 12 years of experience in the field.

The journey toward parenthood can be fraught with challenges, especially for couples dealing with infertility. IVF offers hope by allowing fertilization to occur outside the body, providing an opportunity to select high-quality embryos for transfer into the uterus. However, not all embryos are created equal; their quality can significantly impact the likelihood of successful implantation and pregnancy.

Dr Pavan Devendra Bendale is recognized as an IVF specialist in Chinchwad, providing expert care and guidance to couples throughout their fertility journeys. His extensive background in reproductive medicine equips him with the knowledge and skills necessary to navigate the complexities of IVF, ensuring that patients receive personalized treatment plans tailored to their unique needs.

The Role of Embryo Quality in IVF Success Rates”

Embryo quality refers to the developmental potential of an embryo, which is assessed through various grading systems based on morphological characteristics. The grading process typically occurs at different stages of embryo development:

Day 3 Embryos: At this stage, embryos are usually assessed for cell number and fragmentation:

Grade 1: 6-8 cells with minimal fragmentation (less than 10%).

Grade 2: 6-8 cells with moderate fragmentation (10-25%).

Grade 3: Less than 6 cells or significant fragmentation (greater than 25%).

Day 5 Blastocysts: By this stage, embryos are evaluated based on their inner cell mass (ICM) and trophectoderm (TE):

Grade A: Many tightly packed cells indicating high implantation potential.

Grade B: Loosely packed cells suggesting moderate potential.

Grade C: Poorly formed layers with low implantation potential.

Research has consistently shown that higher-quality embryos correlate with increased pregnancy and live birth rates. For instance, studies indicate that embryos graded as AA have a pregnancy rate of approximately 65%, while those graded as BB may only achieve a pregnancy rate of around 30%.

Factors Influencing Embryo Quality:

Several factors affect embryo quality, including:

Maternal Age: Age is one of the most significant factors influencing embryo quality. As women age, particularly after age 35, both the quantity and quality of eggs decline due to natural aging processes. This decline directly impacts embryo quality and subsequent IVF success rates.

Ovarian Reserve: The number and quality of eggs retrieved during ovarian stimulation are crucial for determining embryo quality. Tests such as antral follicle count and hormone assessments can provide insights into ovarian reserve but do not definitively predict egg quality.

Laboratory Conditions: The environment in which embryos are cultured significantly affects their development. Advanced laboratory techniques and optimal culture conditions are essential for maintaining embryo viability.

Genetic Factors: The genetic makeup of both sperm and egg influences embryo quality. Chromosomal abnormalities can lead to lower-quality embryos that may not implant successfully.

Fragmentation Levels: Fragmentation refers to cellular debris within an embryo; lower fragmentation levels are associated with higher implantation rates.

Preimplantation Genetic Testing (PGT):

To enhance the chances of successful pregnancies, many fertility clinics offer Preimplantation Genetic Testing (PGT). This involves testing embryos for chromosomal normalcy before transfer:

PGT-A (Preimplantation Genetic Testing for Aneuploidy): Identifies chromosomal abnormalities in embryos.

PGT-M (Preimplantation Genetic Testing for Monogenic Disorders): Screens for specific genetic disorders.

Embryos that pass PGT-A are more likely to result in successful pregnancies compared to unscreened embryos. This testing allows couples to select the healthiest embryos for transfer, thereby improving overall success rates.

Emotional and Psychological Considerations:

The journey through IVF can be emotionally taxing for couples. Understanding how embryo quality affects success rates can help manage expectations:

Setting Realistic Expectations: Couples should be aware that even high-quality embryos do not guarantee success due to various factors beyond their control.

Support Systems: Emotional support from partners, family, or counselling services can help couples navigate the ups and downs of fertility treatments.

Dr Pavan Devendra Bendale’s extensive experience as an IVF specialist in Chinchwad allows him to guide couples through their fertility journeys with personalized care and advanced medical techniques. His approach emphasizes:

Comprehensive Evaluations: Conduct thorough assessments to identify underlying issues affecting fertility.

Patient-Centric Care: Ensuring open communication and a supportive environment throughout treatment.

Advanced Technology: Utilizing cutting-edge technology and techniques in his practice to enhance treatment outcomes.

Dr. Bendale’s commitment to patient care is evident in his successful track record of helping couples achieve their dreams of parenthood through tailored treatment plans that prioritize both physical health and emotional well-being.

In conclusion, the quality of embryos is a pivotal factor influencing the success rates of IVF procedures. High-quality embryos increase the likelihood of achieving pregnancy and live births while also reducing the risk of miscarriage. Factors such as maternal age, ovarian reserve, laboratory conditions, and genetic integrity play vital roles in determining embryo quality.

For those considering IVF or seeking expert guidance on their fertility journey, consulting with a qualified specialist like Dr Pavan Devendra Bendale can provide invaluable support and increase the chances of successful outcomes in achieving their dreams of starting a family.

Understanding the importance of embryo quality not only empowers couples but also helps them maintain realistic expectations throughout their journey toward parenthood. With His expertise as an IVF specialist in Chinchwad, couples can navigate this complex process with confidence and hope for a positive outcome in their fertility endeavours.