Ran Li - Academia.edu (original) (raw)

Papers by Ran Li

Research paper thumbnail of A rare case of giant extra-ovarian mucinous cystadenoma arising from sigmoid mesocolon

Journal of surgical case reports, 2018

An 80-year-old female presented with one month history of acutely worsening abdominal distention ... more An 80-year-old female presented with one month history of acutely worsening abdominal distention and pain, without features of bowel obstruction. A giant intra-abdominal simple cyst, separate from the ovaries, was seen on imaging. Initial haematological and biochemical investigations, including tumour markers, were normal. At laparotomy, the cystic tumour was discovered to arise from the sigmoid mesocolon and was resected . Histopathology revealed the tumour to be a benign extra-ovarian mucinous cystadenoma, which is a neoplasm of ovarian origin that can arise from extra-ovarian sites, including the mesentery. Extra-ovarian mucinous cystadenoma arising specifically from the mesentery are very rare intra-abdominal neoplasms with malignant potential despite its benign appearance on investigations. This case aims to raise awareness of this condition and to highlight its diagnostic approach and surgical management.

Research paper thumbnail of Evaluating the learning curve for posterior retroperitoneoscopic adrenalectomy

Annals of Laparoscopic and Endoscopic Surgery, 2017

Research paper thumbnail of The pharmacology of Malo maxima jellyfish venom extract in isolated cardiovascular tissues: A probable cause of the Irukandji syndrome in Western Australia

Toxicology Letters, 2011

The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspec... more The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspected of causing Irukandji syndrome in the Broome region of Western Australia, was investigated in rat tissues. In left atria, M. maxima crude venom extract (CVE; 1-100 g/mL) caused concentration-dependent inotropic responses which were unaffected by atropine (1 M), but significantly attenuated by tetrodotoxin (TTX; 0.1 M), propranolol (1 M), Mg 2+ (6 mM) or calcitonin gene-related peptide antagonist (CGRP 8-37 ; 1 M). CVE caused no change in right atrial rate until 100 g/mL, which elicited bradycardia. This was unaffected by atropine, TTX, propranolol or CGRP 8-37. In the presence of Mg 2+ , CVE 30-100 g/mL caused tachycardia. In small mesenteric arteries CVE caused concentration-dependent contractions (pEC 50 1.03 ± 0.07 g/mL) that were unaffected by prazosin (0.3 M),-conotoxin GVIA (0.1 M) or Mg 2+ (6 mM). There was a 2-fold increase in sensitivity in the presence of CGRP 8-37 (3 M). TTX (0.1 M), box jellyfish Chironex fleckeri antivenom (92.6 U/mL) and benextramine (3 M) decreased sensitivity by 2.6, 1.9 and 2.1-fold, respectively. CVE-induced maximum contractions were attenuated by C. fleckeri antivenom (−22%) or benextramine (−49%). M. maxima CVE appears to activate the sympathetic, but not parasympathetic, nervous system and to stimulate sensory nerve CGRP release in left atria and resistance arteries. These effects are consistent with the catecholamine excess thought to cause Irukandji syndrome, with additional actions of CGRP release.

Research paper thumbnail of Australian carybdeid jellyfish causing "Irukandji syndrome

Research paper thumbnail of The pharmacology of Malo maxima jellyfish venom extract in isolated cardiovascular tissues: A probable cause of the Irukandji syndrome in Western Australia

Toxicology Letters, 2011

The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspec... more The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspected of causing Irukandji syndrome in the Broome region of Western Australia, was investigated in rat tissues. In left atria, M. maxima crude venom extract (CVE; 1-100 g/mL) caused concentration-dependent inotropic responses which were unaffected by atropine (1 M), but significantly attenuated by tetrodotoxin (TTX; 0.1 M), propranolol (1 M), Mg 2+ (6 mM) or calcitonin gene-related peptide antagonist (CGRP 8-37 ; 1 M). CVE caused no change in right atrial rate until 100 g/mL, which elicited bradycardia. This was unaffected by atropine, TTX, propranolol or CGRP 8-37 . In the presence of Mg 2+ , CVE 30-100 g/mL caused tachycardia. In small mesenteric arteries CVE caused concentration-dependent contractions (pEC 50 1.03 ± 0.07 g/mL) that were unaffected by prazosin (0.3 M), -conotoxin GVIA (0.1 M) or Mg 2+ (6 mM). There was a 2-fold increase in sensitivity in the presence of CGRP 8-37 (3 M). TTX (0.1 M), box jellyfish Chironex fleckeri antivenom (92.6 U/mL) and benextramine (3 M) decreased sensitivity by 2.6, 1.9 and 2.1-fold, respectively. CVE-induced maximum contractions were attenuated by C. fleckeri antivenom (−22%) or benextramine (−49%). M. maxima CVE appears to activate the sympathetic, but not parasympathetic, nervous system and to stimulate sensory nerve CGRP release in left atria and resistance arteries. These effects are consistent with the catecholamine excess thought to cause Irukandji syndrome, with additional actions of CGRP release.

Research paper thumbnail of A rare case of giant extra-ovarian mucinous cystadenoma arising from sigmoid mesocolon

Journal of surgical case reports, 2018

An 80-year-old female presented with one month history of acutely worsening abdominal distention ... more An 80-year-old female presented with one month history of acutely worsening abdominal distention and pain, without features of bowel obstruction. A giant intra-abdominal simple cyst, separate from the ovaries, was seen on imaging. Initial haematological and biochemical investigations, including tumour markers, were normal. At laparotomy, the cystic tumour was discovered to arise from the sigmoid mesocolon and was resected . Histopathology revealed the tumour to be a benign extra-ovarian mucinous cystadenoma, which is a neoplasm of ovarian origin that can arise from extra-ovarian sites, including the mesentery. Extra-ovarian mucinous cystadenoma arising specifically from the mesentery are very rare intra-abdominal neoplasms with malignant potential despite its benign appearance on investigations. This case aims to raise awareness of this condition and to highlight its diagnostic approach and surgical management.

Research paper thumbnail of Evaluating the learning curve for posterior retroperitoneoscopic adrenalectomy

Annals of Laparoscopic and Endoscopic Surgery, 2017

Research paper thumbnail of The pharmacology of Malo maxima jellyfish venom extract in isolated cardiovascular tissues: A probable cause of the Irukandji syndrome in Western Australia

Toxicology Letters, 2011

The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspec... more The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspected of causing Irukandji syndrome in the Broome region of Western Australia, was investigated in rat tissues. In left atria, M. maxima crude venom extract (CVE; 1-100 g/mL) caused concentration-dependent inotropic responses which were unaffected by atropine (1 M), but significantly attenuated by tetrodotoxin (TTX; 0.1 M), propranolol (1 M), Mg 2+ (6 mM) or calcitonin gene-related peptide antagonist (CGRP 8-37 ; 1 M). CVE caused no change in right atrial rate until 100 g/mL, which elicited bradycardia. This was unaffected by atropine, TTX, propranolol or CGRP 8-37. In the presence of Mg 2+ , CVE 30-100 g/mL caused tachycardia. In small mesenteric arteries CVE caused concentration-dependent contractions (pEC 50 1.03 ± 0.07 g/mL) that were unaffected by prazosin (0.3 M),-conotoxin GVIA (0.1 M) or Mg 2+ (6 mM). There was a 2-fold increase in sensitivity in the presence of CGRP 8-37 (3 M). TTX (0.1 M), box jellyfish Chironex fleckeri antivenom (92.6 U/mL) and benextramine (3 M) decreased sensitivity by 2.6, 1.9 and 2.1-fold, respectively. CVE-induced maximum contractions were attenuated by C. fleckeri antivenom (−22%) or benextramine (−49%). M. maxima CVE appears to activate the sympathetic, but not parasympathetic, nervous system and to stimulate sensory nerve CGRP release in left atria and resistance arteries. These effects are consistent with the catecholamine excess thought to cause Irukandji syndrome, with additional actions of CGRP release.

Research paper thumbnail of Australian carybdeid jellyfish causing "Irukandji syndrome

Research paper thumbnail of The pharmacology of Malo maxima jellyfish venom extract in isolated cardiovascular tissues: A probable cause of the Irukandji syndrome in Western Australia

Toxicology Letters, 2011

The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspec... more The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspected of causing Irukandji syndrome in the Broome region of Western Australia, was investigated in rat tissues. In left atria, M. maxima crude venom extract (CVE; 1-100 g/mL) caused concentration-dependent inotropic responses which were unaffected by atropine (1 M), but significantly attenuated by tetrodotoxin (TTX; 0.1 M), propranolol (1 M), Mg 2+ (6 mM) or calcitonin gene-related peptide antagonist (CGRP 8-37 ; 1 M). CVE caused no change in right atrial rate until 100 g/mL, which elicited bradycardia. This was unaffected by atropine, TTX, propranolol or CGRP 8-37 . In the presence of Mg 2+ , CVE 30-100 g/mL caused tachycardia. In small mesenteric arteries CVE caused concentration-dependent contractions (pEC 50 1.03 ± 0.07 g/mL) that were unaffected by prazosin (0.3 M), -conotoxin GVIA (0.1 M) or Mg 2+ (6 mM). There was a 2-fold increase in sensitivity in the presence of CGRP 8-37 (3 M). TTX (0.1 M), box jellyfish Chironex fleckeri antivenom (92.6 U/mL) and benextramine (3 M) decreased sensitivity by 2.6, 1.9 and 2.1-fold, respectively. CVE-induced maximum contractions were attenuated by C. fleckeri antivenom (−22%) or benextramine (−49%). M. maxima CVE appears to activate the sympathetic, but not parasympathetic, nervous system and to stimulate sensory nerve CGRP release in left atria and resistance arteries. These effects are consistent with the catecholamine excess thought to cause Irukandji syndrome, with additional actions of CGRP release.