[Out-of-hospital cardiac arrest during lockdown]. / Prähospitaler Kreislaufstillstand im Lockdown: Auswirkungen der übergreifenden Infektionspräventionsmaßnahmen während der ersten SARS-CoV-2-Welle.

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread worldwide. Consequences of infection prevention measures during such contagion events can cause disadvantages especially for patients in out-of-hospital cardiac arrest (OHCA). METHODS: Retrospective analysis of OHCAs in one county from January-May in 2018, 2019 and 2020, with the first appearance of the SARS-CoV­2 pandemic in 2020 and a high incidence of the influenza virus in 2018. RESULTS: A total of 497 OHCAs were investigated (2018 n = 173; 2019 n = 149; 2020 n = 175). In this study, a constant resuscitation incidence (85-99 resuscitations/100,000 population/year) and locally typical patients (mean 70 years, 66% male; median PES 3) were found. There were no statistically significant differences in the initial situation of the patients (number of observed OHCAs, frequency of lay resuscitations, suspected causes of OHCAs, initial ECG rhythm) and the treatment course (frequency of return of spontaneous circulation [ROSC]/hospital admission/survival to hospital discharge, neurological outcome). None of the OHCA patients in 2020 tested positive for SARS-CoV­2 and 3 patients in 2018 tested positive for the influenza virus. DISCUSSION: The lockdown during the first wave of SARS-CoV­2 pandemic does not seem to have affected the outcome of OHCA patients without coronavirus disease 2019 (COVID-19) in the end.

Time to change the times? Time of recurrence of ventricular fibrillation during OHCA.

AIM OF THE STUDY: For out-of-hospital-cardiac-arrest (OHCA) due to ventricular fibrillation (VF) guidelines recommend early defibrillation followed by chest compressions for two minutes before analyzing shock success. If rhythm analysis reveals VF again, it is obscure whether VF persisted or reoccurred within the two-minutes-cycle of chest compressions after successful defibrillation. We investigated the time of VF-recurrence in OHCA. METHODS: We examined all cases of OHCA presenting with initial VF rhythm at arrival of ALS-ambulance (Marburg-Biedenkopf-County, 246.648 inhabitants) from January 2014 to March 2018. Three independent investigators analyzed corpuls3® ECG-recordings. We included ECG-data from CPR-beginning until four minutes after the third shock. VF termination was defined as the absence of a VF-waveform within 5 s of shock delivery. VF recurrence was defined as the presence of a VF-waveform in the interval 5 s post shock delivery. RESULTS: We included 185 shocks in 82 patients. 74.1% (n = 137) of all shocks terminated VF, but VF recurred in 81% (n = 111). The median (IQR) time of VF-recurrences was 27 s (13.5 s/80.5 s) after shock. 51.4% (n = 57) of VF-recurrence occurred 5-30 s after shock, 13.5% (n = 15) VF-recurrence occurred 31-60 s after shock, 21.6% (n = 24) of VF-recurrence occurred 61-120 s after shock, 13.5% (n = 15) of VF-recurrence occurred 121-240 s after shock. CONCLUSIONS: Although VF was terminated by defibrillation in 74.1%, VF recurred in 81% subsequent to the chest compression interval. Thus, VF reappears frequently and early. It is unclear to which extend chest compressions influence VF-relapse. Further studies need to re-evaluate the algorithm, timing of antiarrhythmic therapy or novel defibrillation strategies to minimize refibrillation during shockable OHCA.

Hypothermia does not influence liver damage and function in a porcine polytrauma model.

BACKGROUND: Previous studies revealed evidence that induced hypothermia attenuates ischemic organ injuries after severe trauma. In the present study, the effect of hypothermia on liver damage was investigated in a porcine long term model of multi-system injury, consisting of blunt chest trauma, penetrating abdominal trauma, musculoskeletal injury, and hemorrhagic shockMETHODS: In 30 pigs, a standardized polytrauma including blunt chest trauma, penetrating abdominal trauma, musculoskeletal injury, and hemorrhagic shock of 45% of total blood volume was induced. Following trauma, hypothermia of 33∘C was induced for 12 h and intensive care treatment was evaluated for 48 h. As outcome parameters, we assessed liver function and serum transaminase levels as well as a histopathological analysis of tissue samples. A further 10 animals served as controls. RESULTS: Serum transaminase levels were increased at the end of the observation period following hypothermia without reaching statistical significance compared to normothermic groups. Liver function was preserved (p⩽ 0.05) after the rewarming period in hypothermic animals but showed no difference at the end of the observation period. In H&E staining, cell death was slightly increased hypothermic animals and caspase-3 staining displayed tendency towards more apoptosis in hypothermic group as well. CONCLUSIONS: Induction of hypothermia could not significantly improve hepatic damage during the first 48 h following major trauma. Further studies focusing on multi-organ failure including a longer observation period are required to illuminate the impact of hypothermia on hepatic function in multiple trauma patients.

Long-Term Effects of Induced Hypothermia on Local and Systemic Inflammation - Results from a Porcine Long-Term Trauma Model.

BACKGROUND: Hypothermia has been discussed as playing a role in improving the early phase of systemic inflammation. However, information on the impact of hypothermia on the local inflammatory response is sparse. We therefore investigated the kinetics of local and systemic inflammation in the late posttraumatic phase after induction of hypothermia in an established porcine long-term model of combined trauma. MATERIALS & METHODS: Male pigs (35 ± 5kg) were mechanically ventilated and monitored over the study period of 48 h. Combined trauma included tibia fracture, lung contusion, liver laceration and pressure-controlled hemorrhagic shock (MAP < 30 ± 5 mmHg for 90 min). After resuscitation, hypothermia (33°C) was induced for a period of 12 h (HT-T group) with subsequent re-warming over a period of 10 h. The NT-T group was kept normothermic. Systemic and local (fracture hematoma) cytokine levels (IL-6, -8, -10) and alarmins (HMGB1, HSP70) were measured via ELISA. RESULTS: Severe signs of shock as well as systemic and local increases of pro-inflammatory mediators were observed in both trauma groups. In general the local increase of pro- and anti-inflammatory mediator levels was significantly higher and prolonged compared to systemic concentrations. Induction of hypothermia resulted in a significantly prolonged elevation of both systemic and local HMGB1 levels at 48 h compared to the NT-T group. Correspondingly, local IL-6 levels demonstrated a significantly prolonged increase in the HT-T group at 48 h. CONCLUSION: A prolonged inflammatory response might reduce the well-described protective effects on organ and immune function observed in the early phase after hypothermia induction. Furthermore, local immune response also seems to be affected. Future studies should aim to investigate the use of therapeutic hypothermia at different degrees and duration of application.

Impact of haemorrhagic shock intensity on the dynamic of alarmins release in porcine poly-trauma animal model.

PURPOSE: Traumatic insults result in an altered inflammatory response, in which alarmins release has a central role. The impact of haemorrhagic shock intensity on the long-term kinetics of alarmins is not yet fully elucidated. We investigated these aspects in a combined trauma (chest, abdominal, and extremities injury) porcine model with different severities and durations of haemorrhagic shock. METHODS: After induction of combined trauma (tibia fracture, lung contusion, and liver laceration), haemorrhagic shock was induced at different intensities: moderate haemorrhage (MH; n = 15): mean arterial pressure (MAP) <30 ± 5 mmHg [maximum loss of total blood volume (TBVmax): 45 %] for 90 min, and severe haemorrhage (SH; n = 10): MAP <25 ± 5 mmHg (TBVmax 50 %) for 120 min. Resuscitation was performed using a standardized crystalloid infusion protocol. Animals were mechanically ventilated and underwent ICU-monitoring for 48 h (MH) and 48.5 h (SH). Blood samples were collected over the clinical time course, and systemic levels of serum alarmins [High-Mobility Group Protein B-1 (HMGB-1) and Heat Shock Protein 70 (HSP70)] were measured using an ELISA kit. RESULTS: Heart rate, systemic blood pressure, lactate, and base excess were significantly altered as a function of haemorrhagic shock in both trauma groups (MH and SH). Systemic HMGB-1 levels were significantly elevated in both trauma groups when compared to the sham group. Haemorrhagic shock severity and duration were positively correlated with HMGB-1 levels and compared to baseline values, concentrations remained significantly increased in SH when compared to MH. On the other hand, we observed a significant decrease in the systemic HSP70 levels of trauma groups (MH, and SH) when compared to the sham group, which was significantly decreased compared to baseline values in SH over the entire time course. CONCLUSION: Our data show that haemorrhagic shock duration and severity affect the systemic levels of HMGB-1 and HSP70. This early alarmins release after trauma can be used to guide the treatment strategies (e.g. surgical procedures) of polytrauma patients.

A porcine polytrauma model with two different degrees of hemorrhagic shock: outcome related to trauma within the first 48 h.

BACKGROUND: An animal polytrauma model was developed, including trunk and extremity injuries combined with hemorrhagic shock and a prolonged post-traumatic phase. This could be useful for the assessment of different therapeutic approaches during intensive care therapy. METHODS: A standardized polytrauma including lung contusion, liver laceration and lower leg fracture was applied in 25 pigs. They underwent controlled haemorrhage either with a blood volume loss of 45 % and a median arterial pressure (MAP) <30 mmHg/90 min (group L, n = 15) or a 50 % blood loss of and an MAP <25 mmHg/120 min (group H, n = 10). Five non-traumatized pigs served as a control (group C). Subsequently, intensive care treatment was given for an observational period of 48 h. RESULTS: Both trauma groups showed signs of shock and organ injury (heart rate, MAP and lactate). The frequency of cardiopulmonary resuscitation (CPR) and lung injury was directly related to the severity of the haemorrhagic shock (CPR-group L: 4 of 15 pigs, group H: 4 of 10 pigs; Respiratory failure-group L: 3 of 13, group H: 3 of 9. There was no difference in mortality between trauma groups. CONCLUSION: The present data suggest that our model reflects the mortality and organ failure of polytrauma in humans during shock and the intensive care period. This suggests that the experimental protocol could be useful for the assessment of therapeutic approaches during the post-traumatic period.

Local inflammation in fracture hematoma: results from a combined trauma model in pigs.

Background. Previous studies showed significant interaction between the local and systemic inflammatory response after severe trauma in small animal models. The purpose of this study was to establish a new combined trauma model in pigs to investigate fracture-associated local inflammation and gain information about the early inflammatory stages after polytrauma. Material and Methods. Combined trauma consisted of tibial fracture, lung contusion, liver laceration, and controlled hemorrhage. Animals were mechanically ventilated and under ICU-monitoring for 48 h. Blood and fracture hematoma samples were collected during the time course of the study. Local and systemic levels of serum cytokines and diverse alarmins were measured by ELISA kit. Results. A statistical significant difference in the systemic serum values of IL-6 and HMGB1 was observed when compared to the sham. Moreover, there was a statistical significant difference in the serum values of the fracture hematoma of IL-6, IL-8, IL-10, and HMGB1 when compared to the systemic inflammatory response. However a decrease of local proinflammatory concentrations was observed while anti-inflammatory mediators increased. Conclusion. Our data showed a time-dependent activation of the local and systemic inflammatory response. Indeed it is the first study focusing on the local and systemic inflammatory response to multiple-trauma in a large animal model.

[Diagnostic image (347). A man with a swelling underneath his tongue]. / Diagnose in beeld (347). Een man met een zwelling onder zijn tong.

A 23-year-old man presented with a painless, growing swelling underneath his tongue due to a ranula, i.e. accumulation of saliva in the drainage canal of the sublingual salivary gland.

Dysregulation of renal sodium transporters in gentamicin-treated rats.

We aimed to investigate the molecular mechanisms underlying the renal wasting of Na(+), K(+), Ca(2+), and Mg(2+) in gentamicin (GM)-treated rats. Male Wistar rats were injected with GM (40 or 80 mg/kg/day for 7 days, respectively; GM-40 or GM-80). The expression of NHE3, Na-K-ATPase, NKCC2, ROMK, NCC, alpha-, beta- and gamma-ENaC, and CaSR was examined in the kidney by immunoblotting and immunohistochemistry. Urinary fractional excretion of Na(+), K(+), Ca(2+), and Mg(2+) was increased and urinary concentration was decreased in both GM-40 and GM-80 rats. In cortex and outer stripe of outer medulla (cortex) in GM-80 rats, the expression of NHE3, Na-K-ATPase, and NKCC2 was decreased; NCC expression was unchanged; and CaSR was upregulated compared to controls. In the inner stripe of outer medulla (ISOM) in GM-80 rats, NKCC2 and Na-K-ATPase expression was decreased, whereas CaSR was upregulated, and NHE3 and ROMK expression remained unchanged. In GM-40 rats, NKCC2 expression was decreased in the cortex and ISOM, whereas NHE3, Na-K-ATPase, CaSR, ROMK, and NCC abundance was unchanged in both cortex and ISOM. Immunoperoxidase labeling confirmed decreased expression of NKCC2 in the thick ascending limb (TAL) in both GM-80- and GM-40-treated rats. Immunoblotting and immunohistochemical analysis revealed increased expression of alpha-, beta-, and gamma-ENaC in cortex in GM-80 rats, but not in GM-40 rats. These findings suggest that the decrease in NKCC2 in TAL seen in response to low-dose (40 mg/kg/day) gentamicin treatment may play an essential role for the increased urinary excretion of Mg(2+) and Ca(2+), and play a significant role for the development of the urinary concentrating defect, and increased urinary excretion of Na(+) and K(+). At high-dose gentamicin, both proximal and TAL sodium transporter downregulation is likely to contribute to this.

Biphasic changes of epithelial sodium channel abundance and trafficking in common bile duct ligation-induced liver cirrhosis.

We hypothesize that dysregulation of the epithelial sodium channel (ENaC) may be responsible for the increased sodium retention in liver cirrhosis. Liver cirrhosis was induced by common bile duct ligation (CBDL). We examined the abundance of ENaC subunits and type 2 isoform of 11beta-hydroxysteroid dehydrogenase (11betaHSD2) in the kidney by immunoblotting and immunohistochemistry at 6 or 8 weeks after operation. At 6 weeks, cirrhotic rats had developed ascites and displayed a positive sodium balance. The urinary sodium excretion and fractional excretion of sodium were decreased, while plasma aldosterone was unchanged. The abundance of ENaC subunits was not changed in the cortex and outer stripe of the outer medulla (OSOM). In contrast, immunoperoxidase microscopy revealed an increased apical targeting of alpha-, beta- and gammaENaC in late distal convoluted tubule, connecting tubule and collecting duct. Moreover, 11betaHSD2 abundance was decreased in the cortex/OSOM and inner stripe of the outer medulla. At 8 weeks, urinary sodium excretion and fractional excretion of sodium were not changed, while the plasma aldosterone level was decreased. The expression of ENaC subunits was decreased in the cortex/OSOM. Immunoperoxidase microscopy confirmed decreased expression of ENaC subunits, whereas subcellular localization was not changed. These results suggest that increased apical targeting of ENaC subunits and diminished abundance of 11betaHSD2 may contribute to promote sodium retention in the sodium-retaining stage of liver cirrhosis (at 6 weeks). The subsequent decreased expression and reduced targeting of ENaC subunits may play a role in promoting sodium excretion in the later stage of liver cirrhosis (at 8 weeks).

Multiple strategies of schistosomes to meet their requirements in the intermediate snail host.

The results of the studies on our model combination Trichobilharzia ocellata-Lymnaea stagnalis, presented in this review, lead to the conclusion that schistosomes use multiple strategies to reach their goals, i.e. to propagate and to continue their life cycle. They have to escape from being attacked by the internal defence system (IDS) of the snail host and to profoundly affect the host's energy flow, of which reproduction and growth are the main determinants, for their own benefit. These physiological changes they establish mainly by interfering with the two regulatory systems in the snail host, the IDS and the neuroendocrine system (NES). Moreover, these two regulatory systems clearly interact with each other. Parasitic E/S products affect the host's IDS both in a direct and an indirect way. The neuropeptides or neuropeptide-like substances that are secreted by parasite glands into the host directly suppress haemocyte activity in the snail. The indirect effects include effects of (1) peptides from connective tissue cells and (2) neuropeptides from NES and/or IDS. Parasitic E/S products also induce the effects on energy flow in the host. These E/S products act either directly on a target, as shown for the inhibiting effect of the parasite on the development of the male copulation organ, or on the NES regulating reproductive activity, e.g. on gene expression. Indirect effects of E/S products on the NES (hormone-receptor interaction, electrical activity) are mediated by a factor from connective tissue cells, presumably belonging to the IDS. The physiological changes in the snail host are obviously of vital importance for the parasites, since they make use of different strategies to bring them about.

Risk factors for otitis media with effusion in children 0 to 2 years of age.

PURPOSE: To determine the possible risk factors associated with the occurrence of otitis media with effusion. PATIENTS AND METHODS: Two hundred eighty-nine children born between July 1987 and October 1988 were studied up to the age of 24 months. The enrollment of the children took place during their regular check-up visits at three different health-care centers. RESULTS: Having older sibling was the most important risk factor, for both the time elapsed until the first occurrence and for the probability of otitis media with effusion at each visit. Other significant risk factors for the probability at each visit were: having had acute otitis media before the visit or before the previous visit, age, a positive family history of otitis media, and upper respiratory tract infections (URTI). CONCLUSION: Having older siblings is the most important risk factor for otitis media with effusion in this age group.

Breast-feeding and acute otitis media.

INTRODUCTION: The risk of acute otitis media (AOM) is estimated as a function of a number of covariates, with special emphasis on changes to this risk after breast-feeding is discontinued. MATERIALS AND METHODS: Two hundred eighty-nine children born between July 1987, and October 1988, were studied up to the age of 24 months. The enrollment of the children took place during their regular check-up visits at three different child health care centers. RESULTS: The risk of AOM was significantly decreased until 4 months after breast-feeding was discontinued; then, without the protective effect of breast-feeding, and with increasing months, the children approached the risk level estimated in the group of children who were never breast-fed. Approximately 12 months after breast-feeding was discontinued, the risk was virtually the same as if the child had never been breast-fed. The risk of AOM was also significantly dependent on the infant's number of siblings and socioeconomic status. CONCLUSION: The risk of AOM depends on the number of months an infant is breast-fed and the number of months that pass after breast-feeding is discontinued.

Otitis media, respiratory tract infections and hearing loss in pre-term and low birthweight infants.

In 1983, 1338 liveborn infants with a gestational age of less than 32 weeks and/or a birthweight of less than 1500 g, were enrolled in a national follow-up study in The Netherlands. At the age of 5 years, 966 children were alive. Of these, 927 (96%) were assessed on a home visit 2-6 weeks after their fifth birthday by three specially trained paediatricians. An assessment of ENT morbidity was made and compared with ENT morbidity in full-term children of the same age group. Markedly preterm birth or very low birthweight does not seem to be a risk factor for developing middle ear disease in childhood, however, the rate of ENT problems seems to be higher than in the general population of Dutch pre-school children.

Validity of tympanometry in the diagnosis of middle ear effusion.

A group of 266 children (515 ears), ranging in age from 5 months to 11 years, was studied. These children were candidates for the insertion of ventilation tubes, or adenoidectomy and/or tonsillectomy with myringotomy. Before surgery, tympanometry was performed. The surgical and tympanometric findings were compared afterwards. Two different tympanometers were used (GSI-27A and TYMP-85TT). This study showed a comparable validity of these two tympanometers. The sensitivity and specificity of tympanometry in the age group of 5 months to 2 years did not show a significant difference from that in the age group of 2-12 years. Otoscopy has limited value for the diagnosis of middle ear effusion in this age group.

Hearing loss in very preterm and very low birthweight infants at the age of 5 years in a nationwide cohort.

In a geographically defined population of very preterm and very low birthweight infants (gestational age < 32 weeks and/or birthweight < 1500 g) hearing was evaluated in 890 children by pure-tone audiometry at the age of 5 years. Hearing loss was conductive/unspecified in 123 (13.8%) and sensorineural in 13 (1.5%) children. The prevalence of sensorineural hearing loss was 15 times as high as in 5-7 year old children in the Dutch population at large. The sensorineural hearing loss prevalence in very low birthweight and extremely low birthweight infants was similar. On account of communication disorders 10 (1.1%) children were classified as disabled and 6 (0.7%) as handicapped, following the definitions of the International Classification of Impairments, Disabilities, and Handicaps of the World Health Organisation. Children with conductive hearing loss had a higher risk of impairments, disabilities and handicaps of language and speech development, than children with normal hearing, the difference being statistically significant. The same holds for children with sensorineural hearing loss; moreover they had a significantly higher risk of impairments, disabilities and handicaps of mental development. Overall comparison of children with and without sensorineural hearing loss proved that the children with sensorineural hearing loss had a significantly less favourable outcome, based on 15 perinatal factors simultaneously. The age at which sensorineural hearing loss in very preterm and/or very low birthweight infants is detected has to be improved.

In vitro release of the anti-gonadotropic hormone, schistosomin, from the central nervous system of Lymnaea stagnalis is induced with a methanolic extract of cercariae of Trichobilharzia ocellata.

Infection with digenetic trematodes causes an inhibition or complete cessation of fecundity in their intermediate hosts, freshwater snails. It has been demonstrated in the host-parasite combination Lymnaea stagnalis-Trichobilharzia ocellata that the action of the female gonadotropic hormones upon their target organs is inhibited by the peptide schistosomin. Schistosomin is produced in the central nervous system of the snail and released upon parasitic infection. In order to study the in vitro release of schistosomin, a bioassay was developed. Central nervous systems were incubated with either an acetic acid or a methanolic extract of larval stages of Trichobilharzia ocellata (miracidia, mother sporocysts, cercariae). The incubation media were chromatographed using HPLC and released schistosomin (-like material) was tested for bioactivity in the calfluxin bioassay. The in vitro release of schistosomin was only induced with a methanolic extract of cercariae. The nature of the cercarial factor is discussed.

Trichobilharzia ocellata: influence of infection on the fecundity of its intermediate snail host Lymnaea stagnalis and cercarial induction of the release of schistosomin, a snail neuropeptide antagonizing female gonadotropic hormones.

Subadult and adult specimens of the pond snail Lymnaea stagnalis were infected with the schistosome Trichobilharzia ocellata. Egg production and growth of the snails were monitored over an 8-week period post-infection (p.i.). Snail haemolymph was collected and analysed for the presence of schistosomin, a neuropeptide which antagonizes the action of the snails' female gonadotropic hormones. Snails infected as subadults showed an increase in fecundity during the first 4 weeks p.i. compared with non-infected controls. The possibility is discussed that this increase is caused by an accelerated maturation of the female sex organs due to elevated levels of Dorsal Body Hormone, a female gonadotropic hormone. No difference in fecundity was found between snails infected as adults and control snails during the first 4 weeks p.i. Snails infected as subadults and as adults showed a decrease in fecundity from week 5 p.i. and onwards. This decrease coincided with the appearance of schistosomin in the haemolymph of the snails and with that of differentiating cercariae in the daughter sporocysts. Cercariae are probably involved in the induction of schistosomin release from the snails' CNS into the haemolymph. Snails infected as subadults or as adults grew at approximately the same rate as uninfected snails.

Deposition and reorientation of cellulose microfibrils in elongating cells of Petunia stylar tissue.

According to Roelofsen and Houwink's (1953, Acta Bot. Neerl. 2, 218-225) multinet growth hypothesis, microfibrils originally deposited transversely in the cell wall become gradually reoriented towards more axial orientations during cell elongation. To establish the extent of reorientation, microfibrils were studied during their deposition and elongation, using stylar parenchyma and transmitting tissue cells of Petunia hybrida L. At the inner surface of very young cells, microfibrils were deposited in alternating Z- and S-helical orientations. The following sequence in deposition, from the exterior to the interior side of the wall, could be inferred: Axial: 150°-180° (Z-helical), 0°-30° (S-helical); oblique: 110°-150° (Z-helical), 30°-70° (S-helical); transverse: 90°-110° (Z-helical), 70°-90° (S-helical). With the increasing pitch, the density of the deposited microfibrils increased as well, giving rise to an alternating helical texture. During elongation, only transversely S- and Z-helically oriented microfibrils were deposited and all microfibrils underwent a certain reorientation as described in the multinet growth hypothesis. The texture resembled that of young cells and the wall maintained its thickness. The extent of passive reorientation was in agreement with the theoretical calculations made by Preston.

Delta-bag cell peptide from the egg-laying hormone precursor of Aplysia. Processing, primary structure, and biological activity.

The bag cells of the marine mollusk Aplysia express a gene encoding a 271-residue egg-laying hormone (ELH) precursor that is processed into at least nine peptide products. Four of the peptides have been identified in bag cell releasates and are known to act as nonsynaptic neurotransmitters in the abdominal ganglion. The isolation, primary structure, and proposed biological activity of a fifth peptide product (delta-bag cell peptide (delta-BCP)) from the ELH precursor are described. delta-BCP was established to be a 39-residue peptide: NH2-Asp-Gln-Asp-Glu-Gly-Asn-Phe-Arg-Arg-Phe-Pro-Thr-Asn-Ala-Val-Ser-Met- Ser-Ala-Asp- Glu-Asn-Ser-Pro-Phe-Asp-Leu-Ser-Asn-Glu-Asp-Gly-Ala-Val-Tyr-Gln-Arg- Asp-Leu-COOH. This sequence corresponds to residues 81-119 of the ELH prohormone and shares sequence identity with atrial gland peptides A and B. Significantly, synthetic delta-BCP stimulated Ca2+ uptake into mitochondria of secretory cells in the albumin gland in vitro, suggesting that the peptide regulates the cellular release of perivitelline fluid by the gland. Similar results were obtained with purified peptide A and a shorter version of delta-BCP (delta-BCP-(14-33)). These results indicate that delta-BCP belongs to a family of structurally related peptides with similar pharmacological activities that center at a conserved region of sequence corresponding to delta-BCP-(14-33).