New Proof of Goldbach’s Conjecture

This paper uses graphic method to analyze the mechanism of prime number formation and the periodic characteristics of its multiple in natural numbers.The Goldbach’s conjecture is proved by the analysis diagrams.

Contralateral Tubal Ectopic Pregnancy after Ovulation of Another Side Ovary in Spontaneous Cycles:A Case Report and Review of the Literature

Pregnancies in the same side tube after the same side ovary ovulation are more common. We report an unusual case of contralateral tubal ectopic pregnancy after ovulation of another side ovary in spontaneous cycles. A 32-year-old woman underwent laparoscopic left fallopian tube conservative surgery because of left tubal pregnancy two years ago. She returned to our hospital with a positive pregnancy test and lower abdominal pain 28 d after the dominant follicle discharged in the right side ovary detected by transvaginal ultrasound in spontaneous cycles. Transvaginal ultrasonography revealed no intrauterine gestational sac but a left adnexal mass measuring 2.6 cm X2.5 cm. Videolaparoscopy was performed, and the diagnosis of an ectopic pregnancy in the let fallopian tube was confirmed by pathologic report. Tubal damage is the most important risk factor for tubal ectopic pregnancy. Embryos can be reversely migrated toward fallopian tubes, due to retrograde action of endometrial waves and uterine contractions, that is another necessary reason which contributes to such tubal pregnancy. Total salpingectomy or tubal sterilization is necessary for avoiding repeated tubal ectopic pregnancy.

HPDL deficiency causes a neuromuscular disease by impairing the mitochondrial respiration

Mitochondrial diseases are caused by variants in both mitochondrial and nuclear genomes.A nuclear gene HPDL(4-hydroxyphenylpyruvate dioxygenase-like),which encodes an intermembrane mitochondrial protein,has been recently implicated in causing a neurodegenerative disease characterized by pediatric-onset spastic movement phenotypes.Here,we report six Chinese patients with bi-allelic HPDL pathogenic variants from four unrelated families showing neuropathic symptoms of variable severity,including developmental delay/intellectual disability,spasm,and hypertonia.Seven different pathogenic variants are identified,of which five are novel.Both fibroblasts and immortalized lymphocytes derived from patients show impaired mitochondrial respiratory function,which is also observed in HPDL-knockdown(KD)He La cells.In these He La cells,overexpression of a wild-type HPDL gene can rescue the respiratory phenotype of oxygen consumption rate.In addition,a decreased activity of the oxidative phosphorylation(OXPHOS)complex II is observed in patient-derived lymphocytes and HPDL-KD He La cells,further supporting an essential role of HPDL in the mitochondrial respiratory chain.Collectively,our data expand the clinical and mutational spectra of this mitochondrial neuropathy and further delineate the possible disease mechanism involving the impairment of the OXPHOS complex II activity due to the bi-allelic inactivations of HPDL.