NICU journey part 2

 Seconds became minutes, minutes became hours,hours became a days,days became weeks ,weeks became months .Shivansh was in NICU for complete 100 days .Those 100 days were the worst part of my life .I was helpless,I was hopeless also sometimes .

 I was a mother but my baby could not drink my milk,I was a mother but I couldn't hold my baby for first 15 days, I was a mother but I couldn't see my baby for 4 days 💔 😔. How unlucky I am as a mother. I felt like the most unlucky mother is me .

This photo was taken when shivansh came to warmer after 50 days .As I already shared he was in incubator with ventilators. 

I think what happens to women when they become mothers is that there's something in us that changes completely.The minute I saw the baby out of my body and i looked at his face, i suddenly realized that you're not important anymore in fact no body is important at that point .There's somebody else more important than me my son shivansh. It's the first time in our lives that we realise we love somebody more than ourselves. When that moment happened in my life, for me, there was nothing more important than my child."Not even my parents ,sibling , in laws , friends that time my only focus was shivansh . I was devastated. 

My NICU journey Part1

On 26 th april 2019,Shivansh was in  deep sleep inside my womb.We went for the doppler scan and radiologist Said baby movement is zero .She gave a score 0/10 for baby movement. My gynae by seeing the report got scared and planned for an immediate ceserian.  As shivansh was only 30 weeks and 5 days the NICU team were informed  ,so that they can take the baby  to NICU .

At 8:03pm I delivered shivansh  . I just heard the crying sound and then I was unconscious. I didn't see the baby .NICU team took my baby with ventilator support.My husband after seeing the baby rushed to me and said baby is very pretty and looking like you only .I was dying that time just to see my baby in NICU.After 4 days when I was little better ,sister took me to NICU in wheel chair. 

I went to see my baby on 5 th day in a wheel chair .We need to wear an apron before entering to the baby's room .I entered the room with so many thoughts in my mind.I saw a very tiny baby inside the incubator was sleeping .I just sanitized my hand and open the door to touch the little hand .Suddenly he tightly hold my thumb. I don't know how shivansh knew its me who came to see him ,who came to touch him .

Shivansh body was full of wires,pipes,needles .I felt like why God is so cruel .Why it is happening with my baby ,why he is suffering from so much pain .Just attaching the lists of things which was in shivansh body - 

1.Ventillator pipe for breathing 

2.ECG wires to monitor the heart and pulse rate 

3.Bp wire to monitor the blood pressure 

4.Intravenous (IV) fluid needle 

5. Wire to check the oxygen concentration 

6.feeding pipe in the nose 

7.so many stickers in his face to hold the wires.

8.Continous pricking in hand and leg for so many tests .

9.one wire in stomach to main tain body temperature. 

10.Very very small diaper  xs I think .

I couldn't stand for few minutes as because of jaundice he lost few gms wt and was looking very skinny . I was in deep pain inside. There were so many questions when doc will remove the wires ,pipes, needles ,when I can see my baby face completely without any wires and tubes ,when I can hold him ,when I can take my portable to home .

After 20 days I got the chance to hold my baby .Doc called it KMC (kangaroo mother care).Baby need to be in  close contact with mother body so that baby can get the warm .Kmc improves the survivability rate and improve the weight gain .I used to do KMC for 6 hours in a day . It was very terrifying as I used to hold the baby with all wires ,pipes ,needles .I used to seat like a statue while holding the baby in the fear of may be some wire will come out ,may be  oxygen desaturation will happen .

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UNIT -5 DEVELOPMENTAL BIOLOGY (GURKEN PROTEIN )VERY VERY IMPORTANT TOPIC

The gurken gene of Drosophila melanogaster encodes a protein with homology to the transforming growth factor alpha (TGF-a) class of signaling molecules.

During Drosophila oogenesis, the gurken gene is transcribed in the cells of the germline. The gurken messenger RNA accumulates in the oocyte and is translated throughout oogenesis. The Gurken protein is transported to the oocyte membrane, and activates the Drosophila epidermal growth factor receptor (Egfr, tyrosine kinase receptor which is expressed on the adjacent follicle cells that surround the oocyte. The activation of this major transmembrane receptor regulates the expression of a number of genes in the follicle cells, and thus initiates a series of events that lead to the correct patterning of both the anteroposterior and the dorsoventral axis of the egg and embryo.

(1). Gurken acts as a ligand that is specific to oogenesis. The Gurken protein consists of an extracellular domain, which harbors a single epidermal growth factor (EGF)-like domain, a transmembrane domain, and a short cytoplasmic domain

 (2). It is homologous to the gene spitz of Drosophila, which acts as ligand of Egfr in the embryo and in imaginal discs.

Early in oogenesis, gurken mRNA is found in the developing oocyte, and the Gurken protein accumulates in the oocyte membrane. At this stage, the oocyte occupies only a small part of the volume of the egg chamber, and therefore only a limited number of follicle cells at the posterior of the egg chamber are in contact with the oocyte membrane. In this group of follicle cells, the Egfr is activated by Gurken protein, which results in the specification of these follicle cells as posterior cells. 

If  Gurken protein is absent, and the follicle cells at the posterior end of the egg chamber are not induced to assume a posterior cell fate. They consequently develop as anterior follicle cells, which results in the production of an egg with two anterior ends. The posterior follicle cells normally send a signal back to the oocyte, which organizes the cytoskeleton of the oocyte and specifies the posterior end of the oocyte. In the mutant egg chambers, no such signal is sent from the follicle cells, and the cytoskeleton of the oocyte is misorganized. RNAs such as bicoid or oskar, which should normally be localized to one end of the egg RNA localization are mislocalized in these mutant oocytes, and the embryos that develop inside such eggs have an abnormal antero-posterior pattern .

In midoogenesis -The oocyte has grown .The gurken RNA accumulates in the region around the oocyte nucleus, and the Gurken protein is now found in a very restricted part of the oocyte membrane, directly overlying the oocyte nucleus. At this stage, Gurken activates the Egfr in the lateral follicle cells that contact the oocyte on the side where the nucleus is situated. Activation of the Egfr in these lateral follicle cells induces them to become dorsal follicle cells. In the absence of gurken signaling, the lateral follicle cells develop into ventral follicle cells . The ventral follicle cells normally regulate the production of a ventral signal that activates the Toll receptor protein on the ventral side of the egg and is responsible for inducing ventral cell fates in the developing embryo. In the strong gurken mutants, therefore, the ventralization of the follicle cell epithelium leads to an overproduction of the ventral signal, and consequently to a ventralized embryo.

Gurken signaling presumably leads to the formation of a broad field of dorsal cell fates, but secondary patterning mechanisms appear to operate to lead to the final, complex pattern of cell fates of the mature egg. In addition, gurken signaling also interacts with signaling through decapentaplegic (dpp), a molecule with homology to TGF-b. In follicle cells that receive both the gurken signal and the dpp signal, formation of dorsal appendages is repressed, and formation of operculum cell fate is induced . The regulation of the embryonic ventral signal by activation of Egfr seems, however, to be independent of the production of dorsal anterior follicle cell fates. In situations where ectopic activation of Egfr in follicle cells is induced in parts of the follicle cell epithelium, embryos result that show only regional dorsalization, corresponding to the region of the follicle cell epithelium where Egfr was ectopically activated .

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IMPORTANT COMPONENTS OF ECM (EXTRACELLULAR MATRIX)

Elastin -This insoluble fibrous macromolecule provides the resilience (stretch) of the skin, vessels, and ligaments by associating with collagen fibers to limit stretching and preventing tearing. It is highly hydrophobic (proline and glycine), is not glycosylated or "hydroxylized". It has many crosslinks at the lysine residues to stablize the fibers. 

Fibrilin -Is bound in fibers of microfibril sheaths. The sheaths are composed primarily of this protein.
The elastic fiber is made of two alternating segments of hydrophobicity and alpha-helical segments (alanine/ lysine --> crosslinks)

Integrins-This glycoprotein is a cell receptor that interacts with the surrounding ECM, providing anchor for the cell to the matrix of the collagen + links to peptidoglycans.This transmembrane cell receptor is made of alpha and beta subunits that function in cell signaling (depend on extracell divalent cations) and the regulation of cell cycle, shape, and motility through LINKING the ECM with the actin cytoskeleton.  Integrins can mediate indirect interactions with the cytoplasmic cytoskeleton through intermediary proteins including talin and vinculin.


Selectins-Carbohydrate binding proteins that bind to glycoproteins from other cells, important in WBC extravasation, the movement of them from inside the capillaries into the tissues

Multiadhesive proteins -

Dthrombospondin,tenascin,vitronectn,nidogen/enactin,van willebrand factor ,laminin and fobronectin.

A. Laminin- This is a large adhesive glycoprotein that is a major component of BASAL LAMINA. It has binding domains specific for other actors in the BL, including type IV collagen, heparin sulfate (perlecan), enactin (nidogen), and integrins. It consists of 3 poly peptide chains: alpha, beta, gamma

B.Fibronectin -
This example of an adhesive glycoprotein is found in most ECM and plasma. It binds to collagen and proteoglycans. Type III module contains RGD sequence for binding receptors. Importantly, it exists as a protein dimer, consisting of two nearly identical monomers linked by a pair of disulfide bonds.
Although Fibronectin is produced from one gene, it has highly diverse isoforms due to this mechanism in pre-mRNA.

Examples:
- Soluble plasma fibronectin - component of blood plasma made by liver
- Insoluble cellular fibronectin - component of ECM.

Proteoglycans -

A.Aggrecan -This is a major macromolecule of cartilage (made of several GAGs). Due to extensive hydration, it creates a gel-like matrix. These proteoglycans require a core of Hyaluronan and it binds to TGF-beta to inhibit ECM synthesis.

B.Decorin-Is a ubiquitous proteoglycan wide spread in ECM binds to type 1 collagen fibrils and can limit their size and binds TGF-beta and sequesters it interaction with cells.

C.Perlecan -Type of proteoglycan, found in basal lamina, structural and filtering function in basal lamina, the glycosaminoglycan chains attached to perlecan are responsible for preventing proteins escaping from the serum to the urine during glomerular filtration, is one of the proteins that can be defective in specific form of muscular dystrophy.

Notes on collagen -

http://dnaofbioscience.blogspot.com/2016/10/collagen.html

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DELTA NOTCH SIGNALLING PATHWAY

The Delta-Notch signalling pathway is a highly conserved cellular signaling 

mechanism that is essential for embryonic development .

Notch genes encode for transmembrane protiens, Delta is an example
 of one of the ligands that bind to the extracellular domain of the
 Notch receptor in Drosophila. Delta is a single-pass transmembrane
 protein ligand that is membrane bound. 

Notch signalling determines cell fate of surounding cells by the process of

 lateral inhibition in both vertbrates and invertebrates. 

Different Notch activation results in different biological alterations in

 gene expression. For example in human adult tissue, activation of Notch1 

corresponds to differentiation of T-cells and self-renewal, which path is 

undertaken is dependent on other environmental factors too.

• It involves proteolytic cleavage to release an intracellular fragment (Nicd) that functions to regulate transcription.
• In the nucleus, Nicd displaces a repression complex and, with the DNA-binding CSL (CBF1, Su(H) and LAG-1) protein, recruits . Additional epigenetic cofactors are implicated and recruitment of kinases and ubiquitin ligases probably contribute to rapid turnover of the activator complex.
• Activity of the receptor is also regulated post-translationally. A number of different auxiliary components are implicated, including several ubiquitin ligases and proteins, such as Numb, that have direct links to the endocytic machinery.
• 

  Notch ligands are transmembrane proteins and they require E3 ubiquitin ligases for their activity. The mechanisms whereby the ligands become competent to signal are not yet known, but probably entail endocytosis. Localization and cleavage of ligands might also contribute to their regulation.

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