Chein spasm sona van biography

Greetings to you, my desert sisters—

brides of the desert—

                       warm greetings to you—

a female poet is mixing

with a ladle

            the hellish furnace of Der Zor

and your luminous faces

                       are springing up

one by one

out of the dense smoke—

            help me, o muse of the desert,

            without you

I can’t

            rhyme

            the discordant clatter

            of these bones—

            nor the whisper of the wind

            that can be easily tamed into a song

                                   elsewhere

            listen!

            to my story

buried in silence

greater than God

here—

wasted in the sand

like an eagle’s seed on a stone—

the seed of the most perfect one—

waiting for its hour of bloom

listen! you—

carelessly leaning

against your beloved—

can you listen to my story

without counting the rhymes

of my repeating lines?—

they go back and forth

the wind and the pain are my teachers

both prone to repetition

listen! . . . listen to me!

because

I am the last bride of Der Zor

           my veil—a sandstorm

I run

pulling the desert

like the train

of my bridal dress

I am the runaway virgin—

with murmuring knees

in the sands

the ghost of your dreams

            in a bloody veil

            let no other virgin in the desert

                                  be betrothed after me

I am the last bride of Der Zor

a virgin cut short by a scimitar

with talking jaws

           unspeakable

            buried up to my knees in the sand    

but I wasn’t always like that:

            I was a mermaid before

                       with a varicolored tail

in Armenia stretching from sea to sea          

until the evil

dawn of day

when I shed my scales and

                                   ended up

in this blazing hell

as a refugee inhermeticsocks

I am the virgin—concubine and servant

of the pimp-desert

the seller of women—

I am their gh

Abstract

Skeletal muscle is a major regulator of glycemic control at rest, and glucose utilization increases drastically during exercise. Sustaining a high glucose utilization via glycolysis requires efficient replenishment of NAD in the cytosol. Apoptosis-inducing mitochondrion-associated factor 2 (AIFM2) was previously shown to be a NADH oxidoreductase domain–containing flavoprotein that promotes glycolysis for diet and cold-induced thermogenesis. Here, we find that AIFM2 is selectively and highly induced in glycolytic extensor digitorum longus (EDL) muscle during exercise. Overexpression (OE) of AIFM2 in myotubes is sufficient to elevate the NAD-to-NADH ratio, increasing the glycolytic rate. Thus, OE of AIFM2 in skeletal muscle greatly increases exercise capacity, with increased glucose utilization. Conversely, muscle-specific Aifm2 depletion via in vivo transfection of hairpins against Aifm2 or tamoxifen-inducible haploinsufficiency of Aifm2 in muscles decreases exercise capacity and glucose utilization in mice. Moreover, muscle-specific introduction of NDE1, Saccharomyces cerevisiae external NADH dehydrogenase (NDE), ameliorates impairment in glucose utilization and exercise intolerance of the muscle-specific Aifm2 haploinsufficient mice. Together, we show a novel role for AIFM2 as a critical metabolic regulator for efficient utilization of glucose in glycolytic EDL muscles.

Introduction

Exercise requires a large amount of energy (ATP) for muscle contraction (1). However, the intramuscular stores of ATP are small (1), so ATP needs to be resynthesized to sustain contractile activity for extended periods. Skeletal muscle replenishes ATP by activating the three major energy systems: 1) phosphagen, 2) glycolysis, and 3) mitochondrial respiration (1). The phosphagen system breaks down phosphocreatine and transfers the phosphate group to ADP and is responsible for ATP regeneration during several seconds (1). As exercise continues for >1

SUMMARY

Kingella kingae is a common etiology of pediatric bacteremia and the leading agent of osteomyelitis and septic arthritis in children aged 6 to 36 months. This Gram-negative bacterium is carried asymptomatically in the oropharynx and disseminates by close interpersonal contact. The colonized epithelium is the source of bloodstream invasion and dissemination to distant sites, and certain clones show significant association with bacteremia, osteoarthritis, or endocarditis. Kingella kingae produces an RTX (repeat-in-toxin) toxin with broad-spectrum cytotoxicity that probably facilitates mucosal colonization and persistence of the organism in the bloodstream and deep body tissues. With the exception of patients with endocardial involvement, children with K. kingae diseases often show only mild symptoms and signs, necessitating clinical acumen. The isolation of K. kingae on routine solid media is suboptimal, and detection of the bacterium is significantly improved by inoculating exudates into blood culture bottles and the use of PCR-based assays. The organism is generally susceptible to antibiotics that are administered to young patients with joint and bone infections. β-Lactamase production is clonal, and the local prevalence of β-lactamase-producing strains is variable. If adequately and promptly treated, invasive K. kingae infections with no endocardial involvement usually run a benign clinical course.

INTRODUCTION

In the s Elizabeth O. King, working at the U.S. Centers for Disease Control (CDC) in Atlanta, GA, described a novel bacterial species isolated from human respiratory secretions, blood, and bone and joint exudates (1). The organism, initially assigned to the genus Moraxella and designated Moraxella kingii in honor of King's seminal research, was later placed in a separate genus and renamed Kingella kingae (2).

The interest in K. kingae was initially limited (3–10), and o

Progressive neurodegenerative disease

"Parkinson's" redirects here. For the medical journal, see Parkinson's Disease (journal). For other uses, see Parkinson's (disambiguation).

Medical condition

Parkinson's disease (PD), or simply Parkinson's, is a neurodegenerative disease primarily of the central nervous system, affecting both motor and non-motor systems. Symptoms typically develop gradually, with non-motor issues becoming more prevalent as the disease progresses. Common motor symptoms include tremors, bradykinesia (slowness of movement), rigidity, and balance difficulties, collectively termed parkinsonism. In later stages, Parkinson's disease dementia, falls, and neuropsychiatric problems such as sleep abnormalities, psychosis, mood swings, or behavioral changes may arise.

Most cases of Parkinson's disease are