Grievous hurt

Section 320. Grievous hurt.
The following kinds of hurt only are designated as "grievous"

First. - Emasculation.

Secondly. - Permanent privation of the sight of either eye.

Thirdly- Permanent privation of the hearing of either ear.

Fourthly. - Privation of any member or joint.

Fifthly. -Destruction or permanent impairing of the powers of any member or joint.

Sixthly. - Permanent disfiguration of the head or face.

Seventhly. - Fracture or dislocation of a bone or tooth.

Eighthly. - Any hurt which endangers life or which causes the sufferer to be during the space of twenty days in severe bodily pain, or unable to follow his ordinary pursuits.

--- punishment for grievous hurt is given under section 325 IPC

Muscles Acting On Vocal Cord

Muscles Acting On Vocal Cord

🎈abductor -  posterior cricoarytenoid
🎈adductor- TILAC
Thyroarytenoid
Interarytenoid
Lateral cricoarytenoid
🎈tensor of vocal cord - cricothyroid
Thyroarytenoid
🎈openers of laryngeal inlet - thyroepiglottis
🎈closers of laryngeal inlet - Interarytenoid
Aryepiglottis

Water requirements

Recommended water supply norm (lpcd)

Less than 20,000 populatn
a. Population served by stand posts- 40L

b. Population provided with pipe connections
70

20,000 to Less than 100,000 -- 100L

100,000 to Less than 1,000,000

100 (with no sewerage system)

135 (with sewerage system)

1,000,000 and above-
150L

Rural and hills (per elevation difference of 100 m)

40L or one hand-pump for 250 persons within a walking distance of 1.6 km

Rural – additional water for cattle in Desert Development Programme (DDP) areas.
30L

GENOME-WIDE ASSOCIATION STUDY (GWA STUDY, OR GWAS)

GENOME-WIDE ASSOCIATION STUDY (GWA STUDY, OR GWAS)

• a/k/a whole genome association study (WGA study, or WGAS)
• most common approach of GWA studies is the “case-control setup” which compares two large groups of individuals
• It finds out associations between single-nucleotide polymorphisms (SNPs) and major diseases.
• Used to identify biological pathways; networks underlying complex diseases and in drug development process.
• Normally compare the DNA of two groups of participant i.e.people with disease (cases) and without disease (controls). 
• It can detect significantly “ALTERED ALLELE FREQUENCY” when comparing with healthy controls
• Each person gives DNA-sample; from which millions of genetic variants are read using SNP arrays. If one type of variant (one allele) is more frequent in people with the disease, the SNP is said to be "associated" with the disease.
• associated SNPs are considered to mark a region of human genome which influences risk of disease. 
• GWA studies investigate entire genome

Flow cytometry

Flow cytometry
-----------------------
• Flow cytometry measures multiple characteristics of individual particles flowing in single file in a stream of fluid.
• It provides rapid analysis of multiple characteristics of single cells.
• It can measure following characteristics:
a) Cell size
b) Cytoplasmic complexity
c) DNA or RNA content
d) Wide range of membrane-bound and intracellular proteins.
• Flow cytometry measures optical and fluorescence characteristics of single cells.
• Principle of flow cytometry:
It measure fluorescence intensity produced by fluorescent-labelled antibodies detecting proteins or ligands that bind to specific cell-associated molecules, such as DNA binding by propidium iodide. 
• The direction of light scattered by the cell correlates to: 
a) Forward Scatter (FS) for Cell size.
b) Side Scatter (SS) for density of the cell (Granularity, vacuoles and membrane size).
• Live cells will have more forward scatter(FS) than dead and apoptotic cells.
• Granulocytes or monocytes have more granularity or vacuoles and they will have more side scattering (SS).

• Clinical uses of flow cytometry:
a) Immunology
1) Histocompatibility cross-matching 
2) Transplantation rejection
3) Immunodeficiency studies
4) HLA-B27 detection
5) Lymphocytosis

b) Oncology 
1) DNA content and S phase of tumors 
2) Measurement of proliferation markers e.g. Ki-67.
c) Leukemia and lymphoma phenotyping
d) Reticulocyte enumeration

Courtesy : Devesh Mishra

Hemoglobin

1) Hemoglobin D-Punjab – (α2βD2) 

results from a GAA ->CAA mutation at codon 121 glutamic acid changed to glutamine
most common form is called Hb D-Punjab after the area in India and Pakistan where it is most frequent 
a/k/ as ---- Hb D-Los Angeles 
Hemoglobin D co-migrates with hemoglobin S at alkaline pH
Hb D does not sickle

2) Hemoglobin H (β4) – 
due to 3 alpha gene deletion. 
formed by a tetramer of β chains 
variants of α-thalassemia.
3) Hemoglobin Barts (γ4) –
Due to deletion of all 4 alpha genes
formed by a tetramer of γ chains
variants of α-thalassemia.

4) Hemoglobin S (α2βS2) – 
caused by a point mutation in the β-globin chain of haemoglobin, 
glutamic acid is replaced by valine at the sixth position of β-globin gene (on chromosome 11)
5) Hemoglobin M:-
group of abnormal Hb's in which a single amino acid substitution favors the formation of methemoglobin in spite of normal quantities of methemoglobin reductase.
Strictly speaking, Hb M are Hb's with mutations at the proximal or distal histidyl residues. Other Hb's M tend to favor the Fe(III) state. 
Heterozygotes have congenital methemoglobinemia; the homozygous state of these genes is unknown and is presumably lethal. 
Specific types include: 
Hb MIwate, α87His→Tyr (α chain, position 87, histidine replaced by tyrosine);
Hb M Hyde Park, β92His→Tyr; 
Hb MBoston, α58His→Tyr; 
Hb MSaskatoon, β63His→Tyr; 
Hb MMilwaukee-1, β67Val→Glu.
6) Hemoglobin C:-( Hb C or HbC) 
abnormal hemoglobin in which substitution of a glutamic acid residue with a lysine residue at the 6th position of the β-globin chain has occurred.
7) Hemoglobin (Hb) Q :-
single nucleotide polymorphism occurring in the Hb α-2 chain.
members of Hb Q family share molecular feature-----the replacement of ASPARTIC ACID (Asp) by HISTIDINE (His) at different positions in the amino acid chain.
These include 
1) Hb Q-Thailand (α74 Asp→His), 
2) Q-India (α64 Asp→His) and
3) Q-Iran (α75 Asp→His).

Tuberculosis

TUBERCULOSIS
• It is also known as Koch’s disease.
• They are acid fast due to presence of mycolic acid.
• Virulence factor is “cord factor”
Two types
a) Primary tuberculosis
• Most commonly seen in children
• It is seen in unsensitised and unexposed individuals
• Source of organism is exogenous.
• Most common site is lung.
• most commonly starts as “latent disease”.
• Unilateral hilar lymph enlargement is seen.
• Calcification, Pleural effusion, Erythema nodosum and Phlyctenular conjunctivitis are also seen.

• Some named Lesions are :
1) Ghon’s focus:- 
Subpleural fibrocaseous lesion (consolidation) of lung parenchyma
Most commonly seen at lower part of upper lobe
Microscopically contains epithelioid granulomatous inflammation
2) Ghon’s complex:-
Consists of Subpleural Ghon’s focus and involved lymph nodes.
Ghon's complex found below clavicle.
3) Ranke’s complex :
Ghon’s focus along with fibrosis and calcification.
4) Simon focus 
It is a tuberculous (TB) nodule formed in lung apex. 
Due to spread of primary TB infection from elsewhere in the body to lung apex via bloodstream. 

b) Post-primary (=Secondary) Pulmonary tuberculosis
• Seen in previously sensitized host due to reactivation of latent primary lesions.
• Frequently associated with decreased immune status.
• Pulmonary fibrosis and cavitation are common.
• Lymph node involvement is rare.
• Endobronchial spread along nearby airways is relatively common finding, resulting in relatively well-defined 2-4 mm nodules or branching lesions “tree-in-bud appearance” on CT.
• Tuberculomas and miliary TB are also recognized patterns of secondary TB.
• Lesions seen are 
1) Puhl’s lesion:-
• Lesion in lung apex and supraclavicular.
• No lymph node involvement.
2) Assman focus:
• Infraclavicular lesion of chronic pulmonary T.B.
Miliary pulmonary tuberculosis
• It is uncommon but carries a poor prognosis.
• It represents hematogenous dissemination of an uncontrolled tuberculous infection.
• Most commonly seen post-primary tuberculosis. 
• Miliary deposits appear as 1-3 mm diameter nodules.
• Lesions are
a) Rich focus 
• It is a tuberculous granuloma occurring on brain cortex.
b) Weigert’s focus :
• Subintimal foci in pulmonary vein.
c) Simond’s focus:
• Localized foci in liver.

Congenital tuberculosis
• Infection with tubercle bacilli either during intrauterine life or before complete passage through birth canal is termed as congenital tuberculosis.
• Three possible modes of infection of fetus
1) Hematogenous infection via umbilical vein
2) fetal aspiration of infected amniotic fluid 
3) fetal ingestion of infected amniotic fluid
• Most common site (overall) and most common site for “primary complex” for “congenital Tuberculosis” is Liver.

• Revised criteria for diagnosis of congenital tuberculosis ( by Cantwell ):
Proven tuberculosis lesions in the infant plus one of the following:
1) Lesions occurring in the first week of life
2) A primary hepatic complex
3) Maternal genital tract or placental tuberculosis
4) Exclusion of postnatal transmission by thorough investigation of contacts.